TY  - JOUR
AU  - Panić, Anastasija
AU  - Sudar-Milovanović, Emina
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Soskić, Sanja S.
AU  - Isenović, Esma R.
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10744
AB  - The liver is an organ in which many oxidative processes occur and represents an important target of oxidative stress (OxS). Under physiological conditions of normal mitochondrial homeostasis, hepatocytes effectively remove reactive oxygen species (ROS) by enabling metabolic adaptations and through the antioxidant defence system mechanisms. However, obesity-induced lipid accumulation in the hepatocytes causes significantly elevated production of ROS, reduces oxidative capacity, and increases oxidative stress (OxS). In men, compared with premenopausal women, the development of insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) in obesity are more prevalent, where oestradiol (E2), the most potent female sex steroid, is proposed as the main culprit. Exogenous oestradiol (E2) administration exerts beneficial effects on antioxidant properties, restores total plasma antioxidant capacity and decreases biomarkers of OxS in ovariectomized animal models. Thus, we hypothesized that E2 treatment in states of obesity could have beneficial effects against OxS in the obese male's liver. We assumed that E2 could directly affect the level of OxS by increasing the level/activity of the AOS enzymes, particularly SOD1, SOD2, GPx, and CAT, in obese males' livers. In addition, we assumed that the level of malondialdehyde (MDA) and protein carbonyl content (PCC) in obese males' livers would be reduced after E2 treatment as a result of E2 inhibitory effect on lipid peroxidation and protein oxidation, respectively. To test our hypothesis, we used the liver of a high-fat (HF) diet-fed male Wistar rats as an animal model of obesity, treated with E2 intraperitoneally (40 μg/kg). Preliminary results from this study support our hypothesis that E2 increases liver protein expression of AOS enzymes: SOD1, GPx, and CAT, in control and HF male rats compared with their respective controls. The protein level of SOD2 and CAT activity was increased in HF treated with E2 compared with non-treated HF rats. Moreover, as we expected, E2 administration significantly decreased the MDA level in both E2-treated groups compared to their controls, while the PCC level was significantly decreased in HF treated group compared with untreated HF rats. In conclusion, the preliminary results we obtained in this study indicate that E2 administration can effectively inhibit the OxS-related processes in the liver in HF diet-induced obesity by increasing AOS enzymes levels and CAT activity, and also by decreasing levels of MDA and PCC. A consequence of our hypothesis is that treatment with E2 may be an innovative way to improve obesity-related liver disease prevention and healing. © 2023 Elsevier Ltd
T2  - Medical Hypotheses
T1  - Does oestradiol treatment alleviate obesity-induced oxidative stress in the male liver?
VL  - 174
SP  - 111049
DO  - 10.1016/j.mehy.2023.111049
ER  - 

@article{
author = "Panić, Anastasija and Sudar-Milovanović, Emina and Stanimirović, Julijana and Obradović, Milan M. and Zafirović, Sonja and Soskić, Sanja S. and Isenović, Esma R.",
year = "2023",
abstract = "The liver is an organ in which many oxidative processes occur and represents an important target of oxidative stress (OxS). Under physiological conditions of normal mitochondrial homeostasis, hepatocytes effectively remove reactive oxygen species (ROS) by enabling metabolic adaptations and through the antioxidant defence system mechanisms. However, obesity-induced lipid accumulation in the hepatocytes causes significantly elevated production of ROS, reduces oxidative capacity, and increases oxidative stress (OxS). In men, compared with premenopausal women, the development of insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) in obesity are more prevalent, where oestradiol (E2), the most potent female sex steroid, is proposed as the main culprit. Exogenous oestradiol (E2) administration exerts beneficial effects on antioxidant properties, restores total plasma antioxidant capacity and decreases biomarkers of OxS in ovariectomized animal models. Thus, we hypothesized that E2 treatment in states of obesity could have beneficial effects against OxS in the obese male's liver. We assumed that E2 could directly affect the level of OxS by increasing the level/activity of the AOS enzymes, particularly SOD1, SOD2, GPx, and CAT, in obese males' livers. In addition, we assumed that the level of malondialdehyde (MDA) and protein carbonyl content (PCC) in obese males' livers would be reduced after E2 treatment as a result of E2 inhibitory effect on lipid peroxidation and protein oxidation, respectively. To test our hypothesis, we used the liver of a high-fat (HF) diet-fed male Wistar rats as an animal model of obesity, treated with E2 intraperitoneally (40 μg/kg). Preliminary results from this study support our hypothesis that E2 increases liver protein expression of AOS enzymes: SOD1, GPx, and CAT, in control and HF male rats compared with their respective controls. The protein level of SOD2 and CAT activity was increased in HF treated with E2 compared with non-treated HF rats. Moreover, as we expected, E2 administration significantly decreased the MDA level in both E2-treated groups compared to their controls, while the PCC level was significantly decreased in HF treated group compared with untreated HF rats. In conclusion, the preliminary results we obtained in this study indicate that E2 administration can effectively inhibit the OxS-related processes in the liver in HF diet-induced obesity by increasing AOS enzymes levels and CAT activity, and also by decreasing levels of MDA and PCC. A consequence of our hypothesis is that treatment with E2 may be an innovative way to improve obesity-related liver disease prevention and healing. © 2023 Elsevier Ltd",
journal = "Medical Hypotheses",
title = "Does oestradiol treatment alleviate obesity-induced oxidative stress in the male liver?",
volume = "174",
pages = "111049",
doi = "10.1016/j.mehy.2023.111049"
}

Panić, A., Sudar-Milovanović, E., Stanimirović, J., Obradović, M. M., Zafirović, S., Soskić, S. S.,& Isenović, E. R.. (2023). Does oestradiol treatment alleviate obesity-induced oxidative stress in the male liver?. in Medical Hypotheses, 174, 111049.
https://doi.org/10.1016/j.mehy.2023.111049

Panić A, Sudar-Milovanović E, Stanimirović J, Obradović MM, Zafirović S, Soskić SS, Isenović ER. Does oestradiol treatment alleviate obesity-induced oxidative stress in the male liver?. in Medical Hypotheses. 2023;174:111049.
doi:10.1016/j.mehy.2023.111049 .

Panić, Anastasija, Sudar-Milovanović, Emina, Stanimirović, Julijana, Obradović, Milan M., Zafirović, Sonja, Soskić, Sanja S., Isenović, Esma R., "Does oestradiol treatment alleviate obesity-induced oxidative stress in the male liver?" in Medical Hypotheses, 174 (2023):111049,
https://doi.org/10.1016/j.mehy.2023.111049 . .

TY  - CONF
AU  - Soskić, Sanja
AU  - Obradović, Milan
AU  - Zafirović, Sonja
AU  - Ilinčić, B.
AU  - Čabarkapa, V.
AU  - Stokić, Edita
AU  - Isenović, Esma R.
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12033
AB  - Rad je koncipiran, dizajniran i urađen u Laborastoriji za radiobiologiju i molekularnu genetiku Instituta za nuklearne nauke “Vinča” – Institutom od nacionalnog značaja – Univerziteta u Beogradu u saradnji sa Medicinskim fakultetom Univerziteta u Novom Sadu i Univerzitetskim Kliničkim CentromVojvodine. Uvod i cilj. Reaktivne vrste kiseonika (ROS) imaju mogućnost da reaguju sa biomolekulima ćelija i telesnih tečnosti i da ih menjaju. Oksidativni stres (OxS) nastaje u ćelijskim sistemima u uslovima narušene ravnoteže između stepena produkcije i otklanjanja visokoreaktivnih molekula, odnosno, kada produkcija ROS prevazilazi antioksidativne kapacitete datih sistema. Jedan od parametara OxS je 4-hidroksi 2-nonelan (4-HNE), čija koncentracija predstavlja stepen lipidne peroksidacije. Antioksidativni zaštitni sistem (AOS) nastao je tokom procesa evolucije u aerobnim uslovima kao odgovor na toksično delovanje kiseonika. Postoji više nivoa AOS, kao što su enzimski antioksidanti i neenzimski antioksidanti. Među najznačajnijim komponentama enzimskog AOS su superoksid dismutaza (SOD), katalaza (CAT), glutation peroksidaza (GPx) glutation reduktaza (GR). Cilj rada je bio utvrđivanje promena koncentracije parametra OxS i aktivnosti enzima AOS kod gojaznih ispitanika u odnosu na normalno uhranjene ispitanike. Metode. U studiju je bilo uključeno 67 osoba oba pola, od čega 36 normalno uhranjenih osoba (kontrole) i 31 gojazna osoba. Ukupni antioksidativni status (TAS) test je meren primenom Randox TAS kita sa Troloksom kao ekvivalentnim standardom na novoj generaciji Daytona (RX) automatskom hemijskom analizatoru prema uputstvu Randox Co. Za određivanje aktivnosti SOD, GPx i GR u serumu ispitanika korišćene su kolorimetrijske metode i komercijalno dostupni Randox kitovi (Randox Labs, Crumlin, UK). Za određivanje aktivnosti CAT i za određivanje koncentracije 4-HNE u serumu ispitanika korišćeni su komercijalno dostupni OxiSelect kitovi (Cell Biolabs, Inc., San Diego, USA). Rezultati. Dobijeni rezultati pokazuju da je koncentracija 4-HNE kod gojaznih osoba bila statistički značajno viša za 36% (p<0,001) u odnosu na nivo 4-HNE merenog kod kontrola. Nivo TAS kod gojaznih ispitanika bio je statistički značajno smanjen (p<0,001) u poređenju sa vrednostima za TAS kod kontrolnih ispitanika. Procenat smanjenja aktivnosti enzima AOS kod gojaznih osoba bio je 35% za SOD (p<0,001), 21% za GR (p<0,001) i 29% za GPx (p<0,001). Nije uočena statistički značajna promena za aktivnost CAT između dve ispitivane grupe. Zaključak. Dobijeni rezultati jasno pokazuju da stanje gojaznosti dovodi do smanjenja aktivnosti AOS, kao i povećanja koncentracije markera lipidne peroksidacije. Takođe, dobijeni rezultati sugerišu da bi određivanje enzima AOS i markera lipidne peroksidacije mogli biti jedni od biomarkera predikcije nastanka gojaznosti.
C3  - KES2022 : 8. Kongres endokrinologa Srbije sa međunarodnim učešćem : Program i zbornik sažetaka
T1  - Parametar oksidativnog stresa i enzimi antioksidativne zaštite kod gojaznih osoba u Srbiji
SP  - 98
EP  - 98
UR  - https://hdl.handle.net/21.15107/rcub_vinar_12033
ER  - 

@conference{
author = "Soskić, Sanja and Obradović, Milan and Zafirović, Sonja and Ilinčić, B. and Čabarkapa, V. and Stokić, Edita and Isenović, Esma R.",
year = "2022",
abstract = "Rad je koncipiran, dizajniran i urađen u Laborastoriji za radiobiologiju i molekularnu genetiku Instituta za nuklearne nauke “Vinča” – Institutom od nacionalnog značaja – Univerziteta u Beogradu u saradnji sa Medicinskim fakultetom Univerziteta u Novom Sadu i Univerzitetskim Kliničkim CentromVojvodine. Uvod i cilj. Reaktivne vrste kiseonika (ROS) imaju mogućnost da reaguju sa biomolekulima ćelija i telesnih tečnosti i da ih menjaju. Oksidativni stres (OxS) nastaje u ćelijskim sistemima u uslovima narušene ravnoteže između stepena produkcije i otklanjanja visokoreaktivnih molekula, odnosno, kada produkcija ROS prevazilazi antioksidativne kapacitete datih sistema. Jedan od parametara OxS je 4-hidroksi 2-nonelan (4-HNE), čija koncentracija predstavlja stepen lipidne peroksidacije. Antioksidativni zaštitni sistem (AOS) nastao je tokom procesa evolucije u aerobnim uslovima kao odgovor na toksično delovanje kiseonika. Postoji više nivoa AOS, kao što su enzimski antioksidanti i neenzimski antioksidanti. Među najznačajnijim komponentama enzimskog AOS su superoksid dismutaza (SOD), katalaza (CAT), glutation peroksidaza (GPx) glutation reduktaza (GR). Cilj rada je bio utvrđivanje promena koncentracije parametra OxS i aktivnosti enzima AOS kod gojaznih ispitanika u odnosu na normalno uhranjene ispitanike. Metode. U studiju je bilo uključeno 67 osoba oba pola, od čega 36 normalno uhranjenih osoba (kontrole) i 31 gojazna osoba. Ukupni antioksidativni status (TAS) test je meren primenom Randox TAS kita sa Troloksom kao ekvivalentnim standardom na novoj generaciji Daytona (RX) automatskom hemijskom analizatoru prema uputstvu Randox Co. Za određivanje aktivnosti SOD, GPx i GR u serumu ispitanika korišćene su kolorimetrijske metode i komercijalno dostupni Randox kitovi (Randox Labs, Crumlin, UK). Za određivanje aktivnosti CAT i za određivanje koncentracije 4-HNE u serumu ispitanika korišćeni su komercijalno dostupni OxiSelect kitovi (Cell Biolabs, Inc., San Diego, USA). Rezultati. Dobijeni rezultati pokazuju da je koncentracija 4-HNE kod gojaznih osoba bila statistički značajno viša za 36% (p<0,001) u odnosu na nivo 4-HNE merenog kod kontrola. Nivo TAS kod gojaznih ispitanika bio je statistički značajno smanjen (p<0,001) u poređenju sa vrednostima za TAS kod kontrolnih ispitanika. Procenat smanjenja aktivnosti enzima AOS kod gojaznih osoba bio je 35% za SOD (p<0,001), 21% za GR (p<0,001) i 29% za GPx (p<0,001). Nije uočena statistički značajna promena za aktivnost CAT između dve ispitivane grupe. Zaključak. Dobijeni rezultati jasno pokazuju da stanje gojaznosti dovodi do smanjenja aktivnosti AOS, kao i povećanja koncentracije markera lipidne peroksidacije. Takođe, dobijeni rezultati sugerišu da bi određivanje enzima AOS i markera lipidne peroksidacije mogli biti jedni od biomarkera predikcije nastanka gojaznosti.",
journal = "KES2022 : 8. Kongres endokrinologa Srbije sa međunarodnim učešćem : Program i zbornik sažetaka",
title = "Parametar oksidativnog stresa i enzimi antioksidativne zaštite kod gojaznih osoba u Srbiji",
pages = "98-98",
url = "https://hdl.handle.net/21.15107/rcub_vinar_12033"
}

Soskić, S., Obradović, M., Zafirović, S., Ilinčić, B., Čabarkapa, V., Stokić, E.,& Isenović, E. R.. (2022). Parametar oksidativnog stresa i enzimi antioksidativne zaštite kod gojaznih osoba u Srbiji. in KES2022 : 8. Kongres endokrinologa Srbije sa međunarodnim učešćem : Program i zbornik sažetaka, 98-98.
https://hdl.handle.net/21.15107/rcub_vinar_12033

Soskić S, Obradović M, Zafirović S, Ilinčić B, Čabarkapa V, Stokić E, Isenović ER. Parametar oksidativnog stresa i enzimi antioksidativne zaštite kod gojaznih osoba u Srbiji. in KES2022 : 8. Kongres endokrinologa Srbije sa međunarodnim učešćem : Program i zbornik sažetaka. 2022;:98-98.
https://hdl.handle.net/21.15107/rcub_vinar_12033 .

Soskić, Sanja, Obradović, Milan, Zafirović, Sonja, Ilinčić, B., Čabarkapa, V., Stokić, Edita, Isenović, Esma R., "Parametar oksidativnog stresa i enzimi antioksidativne zaštite kod gojaznih osoba u Srbiji" in KES2022 : 8. Kongres endokrinologa Srbije sa međunarodnim učešćem : Program i zbornik sažetaka (2022):98-98,
https://hdl.handle.net/21.15107/rcub_vinar_12033 .

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Obradović, Milan M.
AU  - Stewart, Alan J.
AU  - Essack, Magbubah
AU  - Pitt, Samantha J.
AU  - Samardžić, Vladimir
AU  - Soskić, Sanja S.
AU  - Gojobori, Takashi
AU  - Isenović, Esma R.
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10047
AB  - Levothyroxine (LT4) is used to treat frequently encountered endocrinopathies such as thyroid diseases. It is regularly used in clinical (overt) hypothyroidism cases and subclinical (latent) hypothyroidism cases in the last decade. Suppressive LT4 therapy is also part of the medical regimen used to manage thyroid malignancies after a thyroidectomy. LT4 treatment possesses dual effects: substituting new-onset thyroid hormone deficiency and suppressing the local and distant malignancy spreading in cancer. It is the practice to administer LT4 in less-than-high suppressive doses for growth control of thyroid nodules and goiter, even in patients with preserved thyroid function. Despite its approved safety for clinical use, LT4 can sometimes induce side-effects, more often recorded with patients under treatment with LT4 suppressive doses than in unintentionally LT4-overdosed patients. Cardiac arrhythmias and the deterioration of osteoporosis are the most frequently documented side-effects of LT4 therapy. It also lowers the threshold for the onset or aggravation of cardiac arrhythmias for patients with pre-existing heart diseases. To improve the quality of life in LT4-substituted patients, clinicians often prescribe higher doses of LT4 to reach low normal TSH levels to achieve cellular euthyroidism. In such circumstances, the risk of cardiac arrhythmias, particularly atrial fibrillation, increases, and the combined use of LT4 and triiodothyronine further complicates such risk. This review summarizes the relevant available data related to LT4 suppressive treatment and the associated risk of cardiac arrhythmia.
T2  - Frontiers in Endocrinology
T1  - Levothyroxine Treatment and the Risk of Cardiac Arrhythmias – Focus on the Patient Submitted to Thyroid Surgery
VL  - 12
SP  - 1415
DO  - 10.3389/fendo.2021.758043
ER  - 

@article{
author = "Gluvić, Zoran and Obradović, Milan M. and Stewart, Alan J. and Essack, Magbubah and Pitt, Samantha J. and Samardžić, Vladimir and Soskić, Sanja S. and Gojobori, Takashi and Isenović, Esma R.",
year = "2021",
abstract = "Levothyroxine (LT4) is used to treat frequently encountered endocrinopathies such as thyroid diseases. It is regularly used in clinical (overt) hypothyroidism cases and subclinical (latent) hypothyroidism cases in the last decade. Suppressive LT4 therapy is also part of the medical regimen used to manage thyroid malignancies after a thyroidectomy. LT4 treatment possesses dual effects: substituting new-onset thyroid hormone deficiency and suppressing the local and distant malignancy spreading in cancer. It is the practice to administer LT4 in less-than-high suppressive doses for growth control of thyroid nodules and goiter, even in patients with preserved thyroid function. Despite its approved safety for clinical use, LT4 can sometimes induce side-effects, more often recorded with patients under treatment with LT4 suppressive doses than in unintentionally LT4-overdosed patients. Cardiac arrhythmias and the deterioration of osteoporosis are the most frequently documented side-effects of LT4 therapy. It also lowers the threshold for the onset or aggravation of cardiac arrhythmias for patients with pre-existing heart diseases. To improve the quality of life in LT4-substituted patients, clinicians often prescribe higher doses of LT4 to reach low normal TSH levels to achieve cellular euthyroidism. In such circumstances, the risk of cardiac arrhythmias, particularly atrial fibrillation, increases, and the combined use of LT4 and triiodothyronine further complicates such risk. This review summarizes the relevant available data related to LT4 suppressive treatment and the associated risk of cardiac arrhythmia.",
journal = "Frontiers in Endocrinology",
title = "Levothyroxine Treatment and the Risk of Cardiac Arrhythmias – Focus on the Patient Submitted to Thyroid Surgery",
volume = "12",
pages = "1415",
doi = "10.3389/fendo.2021.758043"
}

Gluvić, Z., Obradović, M. M., Stewart, A. J., Essack, M., Pitt, S. J., Samardžić, V., Soskić, S. S., Gojobori, T.,& Isenović, E. R.. (2021). Levothyroxine Treatment and the Risk of Cardiac Arrhythmias – Focus on the Patient Submitted to Thyroid Surgery. in Frontiers in Endocrinology, 12, 1415.
https://doi.org/10.3389/fendo.2021.758043

Gluvić Z, Obradović MM, Stewart AJ, Essack M, Pitt SJ, Samardžić V, Soskić SS, Gojobori T, Isenović ER. Levothyroxine Treatment and the Risk of Cardiac Arrhythmias – Focus on the Patient Submitted to Thyroid Surgery. in Frontiers in Endocrinology. 2021;12:1415.
doi:10.3389/fendo.2021.758043 .

Gluvić, Zoran, Obradović, Milan M., Stewart, Alan J., Essack, Magbubah, Pitt, Samantha J., Samardžić, Vladimir, Soskić, Sanja S., Gojobori, Takashi, Isenović, Esma R., "Levothyroxine Treatment and the Risk of Cardiac Arrhythmias – Focus on the Patient Submitted to Thyroid Surgery" in Frontiers in Endocrinology, 12 (2021):1415,
https://doi.org/10.3389/fendo.2021.758043 . .

TY  - JOUR
AU  - Obradović, Milan
AU  - Sudar-Milovanović, Emina
AU  - Soskić, Sanja S.
AU  - Essack, Magbubah
AU  - Arya, Swati
AU  - Stewart, Alan J.
AU  - Gojobori, Takashi
AU  - Isenović, Esma R.
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9833
AB  - The peptide hormone leptin regulates food intake, body mass, and reproductive function and plays a role in fetal growth, proinflammatory immune responses, angiogenesis and lipolysis. Leptin is a product of the obese (ob) gene and, following synthesis and secretion from fat cells in white adipose tissue, binds to and activates its cognate receptor, the leptin receptor (LEP-R). LEP-R distribution facilitates leptin’s pleiotropic effects, playing a crucial role in regulating body mass via a negative feedback mechanism between adipose tissue and the hypothalamus. Leptin resistance is characterized by reduced satiety, over-consumption of nutrients, and increased total body mass. Often this leads to obesity, which reduces the effectiveness of using exogenous leptin as a therapeutic agent. Thus, combining leptin therapies with leptin sensitizers may help overcome such resistance and, consequently, obesity. This review examines recent data obtained from human and animal studies related to leptin, its role in obesity, and its usefulness in obesity treatment.
T2  - Frontiers in Endocrinology
T1  - Leptin and Obesity: Role and Clinical Implication
VL  - 12
SP  - 563
DO  - 10.3389/fendo.2021.585887
ER  - 

@article{
author = "Obradović, Milan and Sudar-Milovanović, Emina and Soskić, Sanja S. and Essack, Magbubah and Arya, Swati and Stewart, Alan J. and Gojobori, Takashi and Isenović, Esma R.",
year = "2021",
abstract = "The peptide hormone leptin regulates food intake, body mass, and reproductive function and plays a role in fetal growth, proinflammatory immune responses, angiogenesis and lipolysis. Leptin is a product of the obese (ob) gene and, following synthesis and secretion from fat cells in white adipose tissue, binds to and activates its cognate receptor, the leptin receptor (LEP-R). LEP-R distribution facilitates leptin’s pleiotropic effects, playing a crucial role in regulating body mass via a negative feedback mechanism between adipose tissue and the hypothalamus. Leptin resistance is characterized by reduced satiety, over-consumption of nutrients, and increased total body mass. Often this leads to obesity, which reduces the effectiveness of using exogenous leptin as a therapeutic agent. Thus, combining leptin therapies with leptin sensitizers may help overcome such resistance and, consequently, obesity. This review examines recent data obtained from human and animal studies related to leptin, its role in obesity, and its usefulness in obesity treatment.",
journal = "Frontiers in Endocrinology",
title = "Leptin and Obesity: Role and Clinical Implication",
volume = "12",
pages = "563",
doi = "10.3389/fendo.2021.585887"
}

Obradović, M., Sudar-Milovanović, E., Soskić, S. S., Essack, M., Arya, S., Stewart, A. J., Gojobori, T.,& Isenović, E. R.. (2021). Leptin and Obesity: Role and Clinical Implication. in Frontiers in Endocrinology, 12, 563.
https://doi.org/10.3389/fendo.2021.585887

Obradović M, Sudar-Milovanović E, Soskić SS, Essack M, Arya S, Stewart AJ, Gojobori T, Isenović ER. Leptin and Obesity: Role and Clinical Implication. in Frontiers in Endocrinology. 2021;12:563.
doi:10.3389/fendo.2021.585887 .

Obradović, Milan, Sudar-Milovanović, Emina, Soskić, Sanja S., Essack, Magbubah, Arya, Swati, Stewart, Alan J., Gojobori, Takashi, Isenović, Esma R., "Leptin and Obesity: Role and Clinical Implication" in Frontiers in Endocrinology, 12 (2021):563,
https://doi.org/10.3389/fendo.2021.585887 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Soskić, Sanja S.
AU  - Stanimirović, Julijana
AU  - Trpković, Andreja
AU  - Jevremović, Danimir P.
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8483
AB  - Cardiovascular (CV) diseases are the most common health problems worldwide, with a permanent increase in incidence. Growing evidence underlines that insulin-like growth factor 1 (IGF-1) is a very important hormone responsible for normal CV system physiology. IGF-1 is an anabolic growth hormone, responsible for cell growth, differentiation, proliferation, and survival. Despite systemic effects, IGF-1 exerts a wide array of influences in the CV system affecting metabolic homeostasis, vasorelaxation, cardiac contractility and hypertrophy, autophagy, apoptosis, and antioxidative processes. The vasodilatory effect of IGF-1, is achieved through the regulation of the activity of endothelial nitric oxide synthase (eNOS) and, at least partly, through enhancing inducible NOS (iNOS) activity. Also, IGF-1 stimulates vascular relaxation through regulation of sodium/potassium-adenosine-triphosphatase. Numerous animal studies provided evidence of diverse influences of IGF-1 in the CV system such as vasorelaxation, anti-apoptotic and prosurvival effects. Human studies indicate that low serum levels of free or total IGF-1 contribute to an increased risk of CV and cerebrovascular disease. Large human trials aiming at finding clinical efficacy and outcome of IGF-1-related therapy are of great interest. We look forward to the development of new IGF 1 therapies with minor side effects. In this review, we discuss the latest literature data regarding the function of IGF-1 in the CV system in the physiological and pathophysiological conditions. © 2019 Bentham Science Publishers.
T2  - Current Pharmaceutical Design
T1  - Effects of IGF-1 on the cardiovascular system
VL  - 25
IS  - 35
SP  - 3715
EP  - 3725
DO  - 10.2174/1381612825666191106091507
ER  - 

@article{
author = "Obradović, Milan M. and Zafirović, Sonja and Soskić, Sanja S. and Stanimirović, Julijana and Trpković, Andreja and Jevremović, Danimir P. and Isenović, Esma R.",
year = "2019",
abstract = "Cardiovascular (CV) diseases are the most common health problems worldwide, with a permanent increase in incidence. Growing evidence underlines that insulin-like growth factor 1 (IGF-1) is a very important hormone responsible for normal CV system physiology. IGF-1 is an anabolic growth hormone, responsible for cell growth, differentiation, proliferation, and survival. Despite systemic effects, IGF-1 exerts a wide array of influences in the CV system affecting metabolic homeostasis, vasorelaxation, cardiac contractility and hypertrophy, autophagy, apoptosis, and antioxidative processes. The vasodilatory effect of IGF-1, is achieved through the regulation of the activity of endothelial nitric oxide synthase (eNOS) and, at least partly, through enhancing inducible NOS (iNOS) activity. Also, IGF-1 stimulates vascular relaxation through regulation of sodium/potassium-adenosine-triphosphatase. Numerous animal studies provided evidence of diverse influences of IGF-1 in the CV system such as vasorelaxation, anti-apoptotic and prosurvival effects. Human studies indicate that low serum levels of free or total IGF-1 contribute to an increased risk of CV and cerebrovascular disease. Large human trials aiming at finding clinical efficacy and outcome of IGF-1-related therapy are of great interest. We look forward to the development of new IGF 1 therapies with minor side effects. In this review, we discuss the latest literature data regarding the function of IGF-1 in the CV system in the physiological and pathophysiological conditions. © 2019 Bentham Science Publishers.",
journal = "Current Pharmaceutical Design",
title = "Effects of IGF-1 on the cardiovascular system",
volume = "25",
number = "35",
pages = "3715-3725",
doi = "10.2174/1381612825666191106091507"
}

Obradović, M. M., Zafirović, S., Soskić, S. S., Stanimirović, J., Trpković, A., Jevremović, D. P.,& Isenović, E. R.. (2019). Effects of IGF-1 on the cardiovascular system. in Current Pharmaceutical Design, 25(35), 3715-3725.
https://doi.org/10.2174/1381612825666191106091507

Obradović MM, Zafirović S, Soskić SS, Stanimirović J, Trpković A, Jevremović DP, Isenović ER. Effects of IGF-1 on the cardiovascular system. in Current Pharmaceutical Design. 2019;25(35):3715-3725.
doi:10.2174/1381612825666191106091507 .

Obradović, Milan M., Zafirović, Sonja, Soskić, Sanja S., Stanimirović, Julijana, Trpković, Andreja, Jevremović, Danimir P., Isenović, Esma R., "Effects of IGF-1 on the cardiovascular system" in Current Pharmaceutical Design, 25, no. 35 (2019):3715-3725,
https://doi.org/10.2174/1381612825666191106091507 . .

TY  - JOUR
AU  - Stokić, Edita
AU  - Kupusinac, Aleksandar
AU  - Tomic-Naglic, Dragana
AU  - Smiljenic, Dragana
AU  - Kovacev-Zavisic, Branka
AU  - Srdić-Galić, Biljana
AU  - Soskić, Sanja S.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1589
T2  - Angiology
T1  - Vitamin D and Dysfunctional Adipose Tissue in Obesity (Authors Reply)
VL  - 68
IS  - 6
SP  - 561
EP  - 561
DO  - 10.1177/0003319717691435
ER  - 

@article{
author = "Stokić, Edita and Kupusinac, Aleksandar and Tomic-Naglic, Dragana and Smiljenic, Dragana and Kovacev-Zavisic, Branka and Srdić-Galić, Biljana and Soskić, Sanja S. and Isenović, Esma R.",
year = "2017",
journal = "Angiology",
title = "Vitamin D and Dysfunctional Adipose Tissue in Obesity (Authors Reply)",
volume = "68",
number = "6",
pages = "561-561",
doi = "10.1177/0003319717691435"
}

Stokić, E., Kupusinac, A., Tomic-Naglic, D., Smiljenic, D., Kovacev-Zavisic, B., Srdić-Galić, B., Soskić, S. S.,& Isenović, E. R.. (2017). Vitamin D and Dysfunctional Adipose Tissue in Obesity (Authors Reply). in Angiology, 68(6), 561-561.
https://doi.org/10.1177/0003319717691435

Stokić E, Kupusinac A, Tomic-Naglic D, Smiljenic D, Kovacev-Zavisic B, Srdić-Galić B, Soskić SS, Isenović ER. Vitamin D and Dysfunctional Adipose Tissue in Obesity (Authors Reply). in Angiology. 2017;68(6):561-561.
doi:10.1177/0003319717691435 .

Stokić, Edita, Kupusinac, Aleksandar, Tomic-Naglic, Dragana, Smiljenic, Dragana, Kovacev-Zavisic, Branka, Srdić-Galić, Biljana, Soskić, Sanja S., Isenović, Esma R., "Vitamin D and Dysfunctional Adipose Tissue in Obesity (Authors Reply)" in Angiology, 68, no. 6 (2017):561-561,
https://doi.org/10.1177/0003319717691435 . .

TY  - THES
AU  - Soskić, Sanja S.
PY  - 2016
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=4822
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:15140/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1025142194
UR  - http://nardus.mpn.gov.rs/123456789/7890
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7317
AB  - Stopa rasta gojaznosti predstavlja glavni javni zdravstveni problem. U Evropi je njena učestalost u opsegu 10-25% kod muškaraca i 10-30% kod žena. Prevalenca gojaznosti je povećana u Srbiji i ona je postala značajan zdravstveni problem kod odraslih u Srbiji: do 54% ispitanika odraslog stanovništva je gojazno. Gojaznost je bolest koja se definiše kao patološka akumulacija telesne masne mase, koja može nastati kao rezultat povećanog unosa energije i smanjene potrošnje energije. Danas se smatra da je genetska predispozicija za nastanak gojaznosti jedan od glavnih faktora rizika za pojedince, ali identifikaciju gena koji su uključeni u nastanak gojaznosti je još uvek teško razjasniti. S obzirom na činjenicu da je koncentracija leptina znatno povećana kod gojaznih osoba, a istovremeno je proporcionalna telesnoj masi, gen leptina (LEP) je procenjivan u odnosu na genetičke varijante koje bi eventualno mogle biti u vezi sa patofiziologijom gojaznosti i njenim komplikacijama. Leptin je hormon protein kodiran genom gojaznosti (ob), a sintetiše ga pretežno belo masno tkivo. Centralni nervni sistem, tačnije jedra hipotalamusa su meta u kojima leptin ispoljava većinu svojih efekata na metabolizam energije. Leptin ostvaruje nekoliko sistemskih efekata kao što: su smanjenje unosa hrane, povećanje energetske potrošnje, kao i smanjenje metaboličke efikasnosti. Pored toga, leptin utiče na širok spektar bioloških funkcija poput metabolizma lipida i glukoze, sintezu glukokortikoida kao i insulina, a postoji sve više dokaza da je leptin uključen i u patogenezu inflamatornih i autoimunih bolesti. Adekvatne masne naslage i koncentracija leptina smanjuju potrebu za unosom hrane, a omogućavaju potrošnju energije putem raznih neuroendokrinih osa i autonomne aktivnosti. Retki sindromi gojaznosti su povezani sa mutacijama LEP gena kod ljudi. Česta genetička varijanta jednog nukleotida u 5 'promotorskom regionu koji se sastoji u supstituciji G u A na nukleotidu (nt) -2548 (LEP G-2548A, -dbSNPID rs7799039) uzvodno od starta transkripcije ATG u promotoru LEP je povezan sa varijacijamakoncentracije leptina u plazmi i indeksom telesne mase (BMI) kod gojaznih osoba...
AB  - The growth in obesity rates presents a major public health concern. In Europe, its prevalence is within the range of 10–25% in men and 10–30% in women. The prevalence of obesity increased in Serbia and it became a significant public health problem among adults: up to 54% examinees of adult populations were obese. Obesity is a disease defined as abnormal accumulation of body fat mass, which may arise as a result of increased energy intake and decreased energy expenditure. Genetic predisposition to obesity has been reported as a major risk factor for individuals, but identification of the involved genes is still difficult to elucidate. Considering the fact that leptin concentration is significantly increased in obese persons and at the same time is proportional with body weight, the leptin gene (LEP) has been evaluated for polymorphisms that could potentially be related to the pathophysiology of obesity and its complications. Leptin is a protein hormone encoded by the obese (ob) gene, and is synthesized predominantly by white adipose cells. Central nervous system, namely hypothalamic nuclei, is the target where leptin exerts most of its effects on energy metabolism. Leptin has several systemic effects such as decreases food intake, increases energy expenditure, and decreases metabolic efficiency. In addition, leptin has been shown to influence a wide spectrum of biological functions, such as lipid and glucose metabolism, synthesis of glucocorticoids as well as insulin, and there is an increasing evidence that leptin is involved in the pathogenesis of inflammatory, and autoimmune diseases. Adequate fat stores and leptin concentrations decrease the need for food intake however, allow expenditure of energy via a variety of neuroendocrine axes, autonomic outputs and activities. Rare obesity syndromes are associated with mutations of LEP in humans. A common single nucleotide polymorphism within the 5′ promoter region consisting in G to A substitution at nucleotide (nt) -2548 (LEP G-2548A, -dbSNPID rs7799039) upstream of the ATG start site, in LEP promoter has been associated with variations in the concentrations of plasma leptin and body mass index (BMI) in obese individuals. It has been shown that LEP G-2548A polymorphism influences expressionand secretion of leptin in adipose tissue...
PB  - Универзитет у Београду, Биолошки факултет
T2  - Универзитет у Београду
T1  - Asocijacija promena antropometrijskih i metaboličkih parametara i aktivnosti enzima antioksidativne zaštite sa polimorfizmom LEP G2548A u genu za leptin kod gojaznih osoba u Srbiji
UR  - https://hdl.handle.net/21.15107/rcub_nardus_7890
ER  - 

@phdthesis{
author = "Soskić, Sanja S.",
year = "2016",
abstract = "Stopa rasta gojaznosti predstavlja glavni javni zdravstveni problem. U Evropi je njena učestalost u opsegu 10-25% kod muškaraca i 10-30% kod žena. Prevalenca gojaznosti je povećana u Srbiji i ona je postala značajan zdravstveni problem kod odraslih u Srbiji: do 54% ispitanika odraslog stanovništva je gojazno. Gojaznost je bolest koja se definiše kao patološka akumulacija telesne masne mase, koja može nastati kao rezultat povećanog unosa energije i smanjene potrošnje energije. Danas se smatra da je genetska predispozicija za nastanak gojaznosti jedan od glavnih faktora rizika za pojedince, ali identifikaciju gena koji su uključeni u nastanak gojaznosti je još uvek teško razjasniti. S obzirom na činjenicu da je koncentracija leptina znatno povećana kod gojaznih osoba, a istovremeno je proporcionalna telesnoj masi, gen leptina (LEP) je procenjivan u odnosu na genetičke varijante koje bi eventualno mogle biti u vezi sa patofiziologijom gojaznosti i njenim komplikacijama. Leptin je hormon protein kodiran genom gojaznosti (ob), a sintetiše ga pretežno belo masno tkivo. Centralni nervni sistem, tačnije jedra hipotalamusa su meta u kojima leptin ispoljava većinu svojih efekata na metabolizam energije. Leptin ostvaruje nekoliko sistemskih efekata kao što: su smanjenje unosa hrane, povećanje energetske potrošnje, kao i smanjenje metaboličke efikasnosti. Pored toga, leptin utiče na širok spektar bioloških funkcija poput metabolizma lipida i glukoze, sintezu glukokortikoida kao i insulina, a postoji sve više dokaza da je leptin uključen i u patogenezu inflamatornih i autoimunih bolesti. Adekvatne masne naslage i koncentracija leptina smanjuju potrebu za unosom hrane, a omogućavaju potrošnju energije putem raznih neuroendokrinih osa i autonomne aktivnosti. Retki sindromi gojaznosti su povezani sa mutacijama LEP gena kod ljudi. Česta genetička varijanta jednog nukleotida u 5 'promotorskom regionu koji se sastoji u supstituciji G u A na nukleotidu (nt) -2548 (LEP G-2548A, -dbSNPID rs7799039) uzvodno od starta transkripcije ATG u promotoru LEP je povezan sa varijacijamakoncentracije leptina u plazmi i indeksom telesne mase (BMI) kod gojaznih osoba..., The growth in obesity rates presents a major public health concern. In Europe, its prevalence is within the range of 10–25% in men and 10–30% in women. The prevalence of obesity increased in Serbia and it became a significant public health problem among adults: up to 54% examinees of adult populations were obese. Obesity is a disease defined as abnormal accumulation of body fat mass, which may arise as a result of increased energy intake and decreased energy expenditure. Genetic predisposition to obesity has been reported as a major risk factor for individuals, but identification of the involved genes is still difficult to elucidate. Considering the fact that leptin concentration is significantly increased in obese persons and at the same time is proportional with body weight, the leptin gene (LEP) has been evaluated for polymorphisms that could potentially be related to the pathophysiology of obesity and its complications. Leptin is a protein hormone encoded by the obese (ob) gene, and is synthesized predominantly by white adipose cells. Central nervous system, namely hypothalamic nuclei, is the target where leptin exerts most of its effects on energy metabolism. Leptin has several systemic effects such as decreases food intake, increases energy expenditure, and decreases metabolic efficiency. In addition, leptin has been shown to influence a wide spectrum of biological functions, such as lipid and glucose metabolism, synthesis of glucocorticoids as well as insulin, and there is an increasing evidence that leptin is involved in the pathogenesis of inflammatory, and autoimmune diseases. Adequate fat stores and leptin concentrations decrease the need for food intake however, allow expenditure of energy via a variety of neuroendocrine axes, autonomic outputs and activities. Rare obesity syndromes are associated with mutations of LEP in humans. A common single nucleotide polymorphism within the 5′ promoter region consisting in G to A substitution at nucleotide (nt) -2548 (LEP G-2548A, -dbSNPID rs7799039) upstream of the ATG start site, in LEP promoter has been associated with variations in the concentrations of plasma leptin and body mass index (BMI) in obese individuals. It has been shown that LEP G-2548A polymorphism influences expressionand secretion of leptin in adipose tissue...",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Asocijacija promena antropometrijskih i metaboličkih parametara i aktivnosti enzima antioksidativne zaštite sa polimorfizmom LEP G2548A u genu za leptin kod gojaznih osoba u Srbiji",
url = "https://hdl.handle.net/21.15107/rcub_nardus_7890"
}

Soskić, S. S.. (2016). Asocijacija promena antropometrijskih i metaboličkih parametara i aktivnosti enzima antioksidativne zaštite sa polimorfizmom LEP G2548A u genu za leptin kod gojaznih osoba u Srbiji. in Универзитет у Београду
Универзитет у Београду, Биолошки факултет..
https://hdl.handle.net/21.15107/rcub_nardus_7890

Soskić SS. Asocijacija promena antropometrijskih i metaboličkih parametara i aktivnosti enzima antioksidativne zaštite sa polimorfizmom LEP G2548A u genu za leptin kod gojaznih osoba u Srbiji. in Универзитет у Београду. 2016;.
https://hdl.handle.net/21.15107/rcub_nardus_7890 .

Soskić, Sanja S., "Asocijacija promena antropometrijskih i metaboličkih parametara i aktivnosti enzima antioksidativne zaštite sa polimorfizmom LEP G2548A u genu za leptin kod gojaznih osoba u Srbiji" in Универзитет у Београду (2016),
https://hdl.handle.net/21.15107/rcub_nardus_7890 .

TY  - JOUR
AU  - Panić, Anastasija
AU  - Soskić, Sanja S.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10315
AB  - Leptin je hormon adipoznog tkiva koji svoje efekte ostvaruje delovanjem na centralni nervni sistem. Leptin se vezuje za svoje OB receptore na neuronima hipotalamusa i posledično suprimira unos hrane i povećava aktivnost simpatičkog nervnog sistema čime stimuliše proces termogeneze i potrošnje energije. Osim što suprimira apetit i stimuliše termogenu potrošnju energije, leptin ostvaruje svoje efekte i na druge organske sisteme, kao što su endokrini, vaskularni, hematopoetski, imunski i mišićnoskeletni, delujući bilo direktno na periferiji organizma, bilo posredstvom centralnog nervnog sistema. Svoje efekte leptin ostvaruje putem veoma rasprostranjene mreže leptinskih receptora, preko nekoliko različitih molekularnih signalnih puteva. Stanje gojaznosti je praćeno povećanjem nivoa leptina u cirkulaciji usled povećane količine masnog tkiva, ali i pored toga, gojazne osobe ispoljavaju rezistenciju na anoreksigenične i metaboličke efekte leptina. Izvestan broj studija je pokazao da leptin može povećati aktivnost simpatičkog nervnog sistema i u netermogenim tkivima glodara dovodeći do hipertenzije usled gojaznosti. Koncept selektivne rezistenicije na leptin predstavlja moguće objašnjenje ovog paradoksa. Još uvek su malobrojne studije u kojima je ispitivan fenomen selektivne leptinske rezistencije kod ljudi. U okviru ovog preglednog članka, dat je prikaz najnovijih saznanja o leptinu, mehanizmu njegovog delovanja kao i o ulozi leptina u patofiziološkim stanjima.
AB  - Leptin is a hormone produced by the adipose tissue, which has effects on the central nervous system. Leptin is bound to its Ob receptor on hypo-thalamic neurons to inhibit feeding behavior and to increase sympathetically-mediated thermogenesis. In addition to anorexia and thermogenesis, leptin also has direct peripheral and central nervous system-mediated effects on the endocrine, vascular, hematopoietc, immune and musculoskeletal systems. Leptin accomplishes its effects using distributed network of leptin receptors and differential molecular signaling pathways. Leptinemia is increased in obesity because of increased adipocyte mass, but obese subjects exhibit resistance to the anorexic and metabolic effects of leptin. However, multiple studies have shown that leptin can increase sympathetic nerve activity to non-thermogenic tissues in rodents causing obesity-related hypertension. One potential explanation of this paradox is selective leptin resistance. Compared with large and persuasive number of studies on the sympathetic and blood pressure effects of leptin in experimental animals, relatively little attention was given to these effects of leptin in humans. This review article presents recent findings related to leptin and its mechanism of action, and also the role of leptin in patophysiological conditions.
T2  - Medicinska istraživanja
T1  - Leptin i mehanizam delovanja leptina
T1  - Leptin and its mechanism of action
VL  - 49
IS  - 2
SP  - 36
EP  - 41
DO  - 10.5937/MedIst1502036P
ER  - 

@article{
author = "Panić, Anastasija and Soskić, Sanja S. and Isenović, Esma R.",
year = "2015",
abstract = "Leptin je hormon adipoznog tkiva koji svoje efekte ostvaruje delovanjem na centralni nervni sistem. Leptin se vezuje za svoje OB receptore na neuronima hipotalamusa i posledično suprimira unos hrane i povećava aktivnost simpatičkog nervnog sistema čime stimuliše proces termogeneze i potrošnje energije. Osim što suprimira apetit i stimuliše termogenu potrošnju energije, leptin ostvaruje svoje efekte i na druge organske sisteme, kao što su endokrini, vaskularni, hematopoetski, imunski i mišićnoskeletni, delujući bilo direktno na periferiji organizma, bilo posredstvom centralnog nervnog sistema. Svoje efekte leptin ostvaruje putem veoma rasprostranjene mreže leptinskih receptora, preko nekoliko različitih molekularnih signalnih puteva. Stanje gojaznosti je praćeno povećanjem nivoa leptina u cirkulaciji usled povećane količine masnog tkiva, ali i pored toga, gojazne osobe ispoljavaju rezistenciju na anoreksigenične i metaboličke efekte leptina. Izvestan broj studija je pokazao da leptin može povećati aktivnost simpatičkog nervnog sistema i u netermogenim tkivima glodara dovodeći do hipertenzije usled gojaznosti. Koncept selektivne rezistenicije na leptin predstavlja moguće objašnjenje ovog paradoksa. Još uvek su malobrojne studije u kojima je ispitivan fenomen selektivne leptinske rezistencije kod ljudi. U okviru ovog preglednog članka, dat je prikaz najnovijih saznanja o leptinu, mehanizmu njegovog delovanja kao i o ulozi leptina u patofiziološkim stanjima., Leptin is a hormone produced by the adipose tissue, which has effects on the central nervous system. Leptin is bound to its Ob receptor on hypo-thalamic neurons to inhibit feeding behavior and to increase sympathetically-mediated thermogenesis. In addition to anorexia and thermogenesis, leptin also has direct peripheral and central nervous system-mediated effects on the endocrine, vascular, hematopoietc, immune and musculoskeletal systems. Leptin accomplishes its effects using distributed network of leptin receptors and differential molecular signaling pathways. Leptinemia is increased in obesity because of increased adipocyte mass, but obese subjects exhibit resistance to the anorexic and metabolic effects of leptin. However, multiple studies have shown that leptin can increase sympathetic nerve activity to non-thermogenic tissues in rodents causing obesity-related hypertension. One potential explanation of this paradox is selective leptin resistance. Compared with large and persuasive number of studies on the sympathetic and blood pressure effects of leptin in experimental animals, relatively little attention was given to these effects of leptin in humans. This review article presents recent findings related to leptin and its mechanism of action, and also the role of leptin in patophysiological conditions.",
journal = "Medicinska istraživanja",
title = "Leptin i mehanizam delovanja leptina, Leptin and its mechanism of action",
volume = "49",
number = "2",
pages = "36-41",
doi = "10.5937/MedIst1502036P"
}

Panić, A., Soskić, S. S.,& Isenović, E. R.. (2015). Leptin i mehanizam delovanja leptina. in Medicinska istraživanja, 49(2), 36-41.
https://doi.org/10.5937/MedIst1502036P

Panić A, Soskić SS, Isenović ER. Leptin i mehanizam delovanja leptina. in Medicinska istraživanja. 2015;49(2):36-41.
doi:10.5937/MedIst1502036P .

Panić, Anastasija, Soskić, Sanja S., Isenović, Esma R., "Leptin i mehanizam delovanja leptina" in Medicinska istraživanja, 49, no. 2 (2015):36-41,
https://doi.org/10.5937/MedIst1502036P . .

TY  - JOUR
AU  - Soskić, Sanja S.
AU  - Panić, Anastasija
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10312
AB  - Prekomerno prisustvo adipoznog tkiva u organizmu, odnosno gojaznost, predstavlja rezultat energetskog disbalansa, pri čemu unos energije premašuje energetsku potrošnju tokom vremena. Gojaznost se smatra hroničnim metaboličkim poremećajem povezanim sa hroničnom niskom inflamacijom okarakterisanom značajnim promenama nivoa adipokina i proinflamatornih citokina, kao i drugih molekula koji utiču na kardiovaskularnu funkciju. Stoga se gojaznost, posebno centralna gojaznost, smatra značajnim faktorom rizika za nastanak kardiovaskularnih bolesti (KVB), među kojima su ateroskleroza i bolest koronarnih arterija, hipertenzija i disfunkcija leve komore. Povećano nakupljanje masnog tkiva oko srca i krvnih sudova, povećani nivo oksidativnog stresa i inflamatorno stanje međusobno interaguju u procesu nastanka KVB. Smanjenje telesne težine može značajno doprineti smanjenju KVB i njihovih komplikacija. U okviru ovog kratkog preglednog članka, dat je prikaz najnovijih literaturnih podataka o uticaju gojaznosti na nastanak kardiovaskularnih poremećaja.
AB  - Obesity is considered to be a chronic metabolic disorder closely connected to the chronically low inflammation characterized by significant changes in the levels of adipokines and proinflammatory cytokines, as well as other molecules that have an impact on cardiovascular function. Therefore, obesity (especially central obesity) is considered to be a significant risk factor for the development of cardiovascular diseases, atherosclerosis, coronary artery disease, hypertension and left ventricular dysfunction being some of them. The increased accumulation of fat tissue around the heart and in the blood vessels, the increased levels of oxidative stress and the inflammatory state mutually interact in the process of cardiovascular disease occurrence. Lowering the amount of body weight could significantly contribute to reduction of cardiovascular diseases and the subsequent complications.
T2  - Medicinska istraživanja
T1  - Efekti gojaznosti na nastanak kardiovaskularnih poremećaja
T1  - The impact of obesity on development of cardiovascular diseases: Mini review
VL  - 49
IS  - 2
SP  - 33
EP  - 35
DO  - 10.5937/MedIst1502033S
ER  - 

@article{
author = "Soskić, Sanja S. and Panić, Anastasija and Isenović, Esma R.",
year = "2015",
abstract = "Prekomerno prisustvo adipoznog tkiva u organizmu, odnosno gojaznost, predstavlja rezultat energetskog disbalansa, pri čemu unos energije premašuje energetsku potrošnju tokom vremena. Gojaznost se smatra hroničnim metaboličkim poremećajem povezanim sa hroničnom niskom inflamacijom okarakterisanom značajnim promenama nivoa adipokina i proinflamatornih citokina, kao i drugih molekula koji utiču na kardiovaskularnu funkciju. Stoga se gojaznost, posebno centralna gojaznost, smatra značajnim faktorom rizika za nastanak kardiovaskularnih bolesti (KVB), među kojima su ateroskleroza i bolest koronarnih arterija, hipertenzija i disfunkcija leve komore. Povećano nakupljanje masnog tkiva oko srca i krvnih sudova, povećani nivo oksidativnog stresa i inflamatorno stanje međusobno interaguju u procesu nastanka KVB. Smanjenje telesne težine može značajno doprineti smanjenju KVB i njihovih komplikacija. U okviru ovog kratkog preglednog članka, dat je prikaz najnovijih literaturnih podataka o uticaju gojaznosti na nastanak kardiovaskularnih poremećaja., Obesity is considered to be a chronic metabolic disorder closely connected to the chronically low inflammation characterized by significant changes in the levels of adipokines and proinflammatory cytokines, as well as other molecules that have an impact on cardiovascular function. Therefore, obesity (especially central obesity) is considered to be a significant risk factor for the development of cardiovascular diseases, atherosclerosis, coronary artery disease, hypertension and left ventricular dysfunction being some of them. The increased accumulation of fat tissue around the heart and in the blood vessels, the increased levels of oxidative stress and the inflammatory state mutually interact in the process of cardiovascular disease occurrence. Lowering the amount of body weight could significantly contribute to reduction of cardiovascular diseases and the subsequent complications.",
journal = "Medicinska istraživanja",
title = "Efekti gojaznosti na nastanak kardiovaskularnih poremećaja, The impact of obesity on development of cardiovascular diseases: Mini review",
volume = "49",
number = "2",
pages = "33-35",
doi = "10.5937/MedIst1502033S"
}

Soskić, S. S., Panić, A.,& Isenović, E. R.. (2015). Efekti gojaznosti na nastanak kardiovaskularnih poremećaja. in Medicinska istraživanja, 49(2), 33-35.
https://doi.org/10.5937/MedIst1502033S

Soskić SS, Panić A, Isenović ER. Efekti gojaznosti na nastanak kardiovaskularnih poremećaja. in Medicinska istraživanja. 2015;49(2):33-35.
doi:10.5937/MedIst1502033S .

Soskić, Sanja S., Panić, Anastasija, Isenović, Esma R., "Efekti gojaznosti na nastanak kardiovaskularnih poremećaja" in Medicinska istraživanja, 49, no. 2 (2015):33-35,
https://doi.org/10.5937/MedIst1502033S . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Stanimirović, Julijana
AU  - Rizzo, Manfredi
AU  - Resanović, Ivana
AU  - Soskić, Sanja S.
AU  - Jevremovic, Danimir
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/613
AB  - The assessment of cardiovascular risk and treatment of cardiovascular diseases are major public health issues worldwide. Inflammation is now recognized as a key regulatory process that links multiple risk factors for atherosclerosis. The substantial number of patients having cardiovascular events lack commonly established risk factors. The utility of high-sensitivity C-reactive protein (hsCRP), a circulating biomarker related to inflammation, may provide additional information in risk prediction. This review will consider the impact of hsCRP level on initiation of statin therapy.
T2  - Angiology
T1  - High-Sensitivity C-Reactive Protein and Statin Initiation
VL  - 66
IS  - 6
SP  - 503
EP  - 507
DO  - 10.1177/0003319714543000
ER  - 

@article{
author = "Trpković, Andreja and Stanimirović, Julijana and Rizzo, Manfredi and Resanović, Ivana and Soskić, Sanja S. and Jevremovic, Danimir and Isenović, Esma R.",
year = "2015",
abstract = "The assessment of cardiovascular risk and treatment of cardiovascular diseases are major public health issues worldwide. Inflammation is now recognized as a key regulatory process that links multiple risk factors for atherosclerosis. The substantial number of patients having cardiovascular events lack commonly established risk factors. The utility of high-sensitivity C-reactive protein (hsCRP), a circulating biomarker related to inflammation, may provide additional information in risk prediction. This review will consider the impact of hsCRP level on initiation of statin therapy.",
journal = "Angiology",
title = "High-Sensitivity C-Reactive Protein and Statin Initiation",
volume = "66",
number = "6",
pages = "503-507",
doi = "10.1177/0003319714543000"
}

Trpković, A., Stanimirović, J., Rizzo, M., Resanović, I., Soskić, S. S., Jevremovic, D.,& Isenović, E. R.. (2015). High-Sensitivity C-Reactive Protein and Statin Initiation. in Angiology, 66(6), 503-507.
https://doi.org/10.1177/0003319714543000

Trpković A, Stanimirović J, Rizzo M, Resanović I, Soskić SS, Jevremovic D, Isenović ER. High-Sensitivity C-Reactive Protein and Statin Initiation. in Angiology. 2015;66(6):503-507.
doi:10.1177/0003319714543000 .

Trpković, Andreja, Stanimirović, Julijana, Rizzo, Manfredi, Resanović, Ivana, Soskić, Sanja S., Jevremovic, Danimir, Isenović, Esma R., "High-Sensitivity C-Reactive Protein and Statin Initiation" in Angiology, 66, no. 6 (2015):503-507,
https://doi.org/10.1177/0003319714543000 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Trpković, Andreja
AU  - Bajić, Vladan P.
AU  - Soskić, Sanja S.
AU  - Jovanović, Aleksandra
AU  - Stanimirović, Julijana
AU  - Panic, Milos
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/281
AB  - C-reactive protein (CRP) is a marker of inflammation. Atherosclerosis is now recognized as inflammatory disease, and it seems that CRP directly contributes to atherogenesis. Oxidation of low-density lipoprotein (LDL) molecule increases the uptake of lipid products by macrophages leading to cholesterol accumulation and subsequent foam cell formation. The elevated levels of high sensitivity CRP (hsCRP) and oxidized LDL (OxLDL) in the blood were found to be associated with cardiovascular diseases (CVD). In this review, we highlighted the evidence that CRP and OxLDL are involved in interrelated (patho) physiological pathways. The findings on association between hsCRP and OxLDL in the clinical setting will be also summarized.
T2  - Clinical Chemistry and Laboratory Medicine
T1  - Interrelatedness between C-reactive protein and oxidized low-density lipoprotein
VL  - 53
IS  - 1
SP  - 29
EP  - 34
DO  - 10.1515/cclm-2014-0590
ER  - 

@article{
author = "Obradović, Milan M. and Trpković, Andreja and Bajić, Vladan P. and Soskić, Sanja S. and Jovanović, Aleksandra and Stanimirović, Julijana and Panic, Milos and Isenović, Esma R.",
year = "2015",
abstract = "C-reactive protein (CRP) is a marker of inflammation. Atherosclerosis is now recognized as inflammatory disease, and it seems that CRP directly contributes to atherogenesis. Oxidation of low-density lipoprotein (LDL) molecule increases the uptake of lipid products by macrophages leading to cholesterol accumulation and subsequent foam cell formation. The elevated levels of high sensitivity CRP (hsCRP) and oxidized LDL (OxLDL) in the blood were found to be associated with cardiovascular diseases (CVD). In this review, we highlighted the evidence that CRP and OxLDL are involved in interrelated (patho) physiological pathways. The findings on association between hsCRP and OxLDL in the clinical setting will be also summarized.",
journal = "Clinical Chemistry and Laboratory Medicine",
title = "Interrelatedness between C-reactive protein and oxidized low-density lipoprotein",
volume = "53",
number = "1",
pages = "29-34",
doi = "10.1515/cclm-2014-0590"
}

Obradović, M. M., Trpković, A., Bajić, V. P., Soskić, S. S., Jovanović, A., Stanimirović, J., Panic, M.,& Isenović, E. R.. (2015). Interrelatedness between C-reactive protein and oxidized low-density lipoprotein. in Clinical Chemistry and Laboratory Medicine, 53(1), 29-34.
https://doi.org/10.1515/cclm-2014-0590

Obradović MM, Trpković A, Bajić VP, Soskić SS, Jovanović A, Stanimirović J, Panic M, Isenović ER. Interrelatedness between C-reactive protein and oxidized low-density lipoprotein. in Clinical Chemistry and Laboratory Medicine. 2015;53(1):29-34.
doi:10.1515/cclm-2014-0590 .

Obradović, Milan M., Trpković, Andreja, Bajić, Vladan P., Soskić, Sanja S., Jovanović, Aleksandra, Stanimirović, Julijana, Panic, Milos, Isenović, Esma R., "Interrelatedness between C-reactive protein and oxidized low-density lipoprotein" in Clinical Chemistry and Laboratory Medicine, 53, no. 1 (2015):29-34,
https://doi.org/10.1515/cclm-2014-0590 . .

TY  - JOUR
AU  - Stokić, Edita
AU  - Kupusinac, Aleksandar
AU  - Tomic-Naglic, Dragana
AU  - Smiljenic, Dragana
AU  - Kovacev-Zavisic, Branka
AU  - Srdić-Galić, Biljana
AU  - Soskić, Sanja S.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/673
AB  - Vitamin D deficiency and dysfunctional adipose tissue are involved in the development of cardiometabolic disturbances (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We evaluated the relation between vitamin D and adipocytokines derived from adipose tissue. We studied 50 obese individuals who were classified into different subgroups according to medians of observed anthropometric parameters (body mass index, body fat percentage, waist circumference, and trunk fat mass). There was a negative correlation between vitamin D level and leptin and resistin (r = -.61, P LT .01), while a positive association with adiponectin concentrations was found (r = .7, P LT .001). Trend estimation showed that increase in vitamin D level is accompanied by intensive increase in adiponectin concentrations (growth coefficient: 12.13). In conclusion, a positive trend was established between vitamin D and the protective adipocytokine adiponectin. The clinical relevance of this relationship needs to be investigated in larger studies.
T2  - Angiology
T1  - Vitamin D and Dysfunctional Adipose Tissue in Obesity
VL  - 66
IS  - 7
SP  - 613
EP  - 618
DO  - 10.1177/0003319714543512
ER  - 

@article{
author = "Stokić, Edita and Kupusinac, Aleksandar and Tomic-Naglic, Dragana and Smiljenic, Dragana and Kovacev-Zavisic, Branka and Srdić-Galić, Biljana and Soskić, Sanja S. and Isenović, Esma R.",
year = "2015",
abstract = "Vitamin D deficiency and dysfunctional adipose tissue are involved in the development of cardiometabolic disturbances (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We evaluated the relation between vitamin D and adipocytokines derived from adipose tissue. We studied 50 obese individuals who were classified into different subgroups according to medians of observed anthropometric parameters (body mass index, body fat percentage, waist circumference, and trunk fat mass). There was a negative correlation between vitamin D level and leptin and resistin (r = -.61, P LT .01), while a positive association with adiponectin concentrations was found (r = .7, P LT .001). Trend estimation showed that increase in vitamin D level is accompanied by intensive increase in adiponectin concentrations (growth coefficient: 12.13). In conclusion, a positive trend was established between vitamin D and the protective adipocytokine adiponectin. The clinical relevance of this relationship needs to be investigated in larger studies.",
journal = "Angiology",
title = "Vitamin D and Dysfunctional Adipose Tissue in Obesity",
volume = "66",
number = "7",
pages = "613-618",
doi = "10.1177/0003319714543512"
}

Stokić, E., Kupusinac, A., Tomic-Naglic, D., Smiljenic, D., Kovacev-Zavisic, B., Srdić-Galić, B., Soskić, S. S.,& Isenović, E. R.. (2015). Vitamin D and Dysfunctional Adipose Tissue in Obesity. in Angiology, 66(7), 613-618.
https://doi.org/10.1177/0003319714543512

Stokić E, Kupusinac A, Tomic-Naglic D, Smiljenic D, Kovacev-Zavisic B, Srdić-Galić B, Soskić SS, Isenović ER. Vitamin D and Dysfunctional Adipose Tissue in Obesity. in Angiology. 2015;66(7):613-618.
doi:10.1177/0003319714543512 .

Stokić, Edita, Kupusinac, Aleksandar, Tomic-Naglic, Dragana, Smiljenic, Dragana, Kovacev-Zavisic, Branka, Srdić-Galić, Biljana, Soskić, Sanja S., Isenović, Esma R., "Vitamin D and Dysfunctional Adipose Tissue in Obesity" in Angiology, 66, no. 7 (2015):613-618,
https://doi.org/10.1177/0003319714543512 . .

TY  - JOUR
AU  - Stokić, Edita
AU  - Kupusinac, Aleksandar
AU  - Tomic-Naglic, Dragana
AU  - Zavisic, Branka Kovacev
AU  - Mitrovic, Milena
AU  - Smiljenic, Dragana
AU  - Soskić, Sanja S.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/395
AB  - Vitamin D deficiency is associated with cardiometabolic risk factors (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We studied 50 obese patients (body mass index [BMI]: 43.5 +/- 9.2 kg/m(2)) and 36 normal weight participants (BMI: 22.6 +/- 1.9 kg/m(2)). The prevalence of vitamin D deficiency (25-hydroxyvitamin D, 25(OH)D LT 50 nmol/L) was 88% among obese patients and 31% among nonobese individuals; 25(OH)D levels were lower in the obese group (27.3 +/- 13.7 vs 64.6 +/- 21.3 nmol/L; P LT .001). There was a negative correlation between vitamin D level and anthropometric indicators of obesity: BMI (r = -0.64; P LT .001), waist circumference (r = -0.59; P LT .001), and body fat percentage (r = -0.64; P LT .001) as well as with fasting plasma insulin (r = -0.35; P LT .001) and homeostasis model assessment of insulin resistance (r = -0.35; P LT .001). In conclusion, we observed a higher prevalence of vitamin D deficiency among obese participants and this was associated with a proatherogenic cardiometabolic risk profile.
T2  - Angiology
T1  - Obesity and Vitamin D Deficiency: Trends to Promote a More Proatherogenic Cardiometabolic Risk Profile
VL  - 66
IS  - 3
SP  - 237
EP  - 243
DO  - 10.1177/0003319714528569
ER  - 

@article{
author = "Stokić, Edita and Kupusinac, Aleksandar and Tomic-Naglic, Dragana and Zavisic, Branka Kovacev and Mitrovic, Milena and Smiljenic, Dragana and Soskić, Sanja S. and Isenović, Esma R.",
year = "2015",
abstract = "Vitamin D deficiency is associated with cardiometabolic risk factors (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We studied 50 obese patients (body mass index [BMI]: 43.5 +/- 9.2 kg/m(2)) and 36 normal weight participants (BMI: 22.6 +/- 1.9 kg/m(2)). The prevalence of vitamin D deficiency (25-hydroxyvitamin D, 25(OH)D LT 50 nmol/L) was 88% among obese patients and 31% among nonobese individuals; 25(OH)D levels were lower in the obese group (27.3 +/- 13.7 vs 64.6 +/- 21.3 nmol/L; P LT .001). There was a negative correlation between vitamin D level and anthropometric indicators of obesity: BMI (r = -0.64; P LT .001), waist circumference (r = -0.59; P LT .001), and body fat percentage (r = -0.64; P LT .001) as well as with fasting plasma insulin (r = -0.35; P LT .001) and homeostasis model assessment of insulin resistance (r = -0.35; P LT .001). In conclusion, we observed a higher prevalence of vitamin D deficiency among obese participants and this was associated with a proatherogenic cardiometabolic risk profile.",
journal = "Angiology",
title = "Obesity and Vitamin D Deficiency: Trends to Promote a More Proatherogenic Cardiometabolic Risk Profile",
volume = "66",
number = "3",
pages = "237-243",
doi = "10.1177/0003319714528569"
}

Stokić, E., Kupusinac, A., Tomic-Naglic, D., Zavisic, B. K., Mitrovic, M., Smiljenic, D., Soskić, S. S.,& Isenović, E. R.. (2015). Obesity and Vitamin D Deficiency: Trends to Promote a More Proatherogenic Cardiometabolic Risk Profile. in Angiology, 66(3), 237-243.
https://doi.org/10.1177/0003319714528569

Stokić E, Kupusinac A, Tomic-Naglic D, Zavisic BK, Mitrovic M, Smiljenic D, Soskić SS, Isenović ER. Obesity and Vitamin D Deficiency: Trends to Promote a More Proatherogenic Cardiometabolic Risk Profile. in Angiology. 2015;66(3):237-243.
doi:10.1177/0003319714528569 .

Stokić, Edita, Kupusinac, Aleksandar, Tomic-Naglic, Dragana, Zavisic, Branka Kovacev, Mitrovic, Milena, Smiljenic, Dragana, Soskić, Sanja S., Isenović, Esma R., "Obesity and Vitamin D Deficiency: Trends to Promote a More Proatherogenic Cardiometabolic Risk Profile" in Angiology, 66, no. 3 (2015):237-243,
https://doi.org/10.1177/0003319714528569 . .

TY  - JOUR
AU  - Soskić, Sanja S.
AU  - Stokić, Edita
AU  - Obradović, Milan M.
AU  - Sudar, Emina
AU  - Tanić, Nasta
AU  - Kupusinac, Aleksandar
AU  - Đorđević, Jelena D.
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/239
AB  - Aim: The aim of this pilot study was to investigate possible associations of LEP promoter polymorphism LEP G-2548A and obesity-associated metabolic and antropometric parameters in obese population. Materials and methods: Group of 31 patients with hyperalimentary type of obesity (mean age: 39.26 +/- 11.45 years; BMI: 41.51 +/- 9.22 kg/m(2)) and 36 healthy, nonobese, normal weight subjects (mean age: 33.55 +/- 6.46 years; BMI: 22.63 +/- 1.94 kg/m(2)) were studied. Blood samples were collected for DNA isolation, serum leptin and serum lipids measurements. LEP G-2548A genotypes were determined by PCR restriction fragment length polymorphism based analyses. Results: No significant differences in genotype and allele frequencies of the LEP G-2548A polymorphism were detected between obese and normal weight subjects. No association was found between this polymorphism and BMI. Obese subjects had statistically significant increase in serum leptin levels compared with control, while no association between leptin concentration and LEP polymorphism LEP G-2548A was found. There is a statistically significant association of LEP G-2548A genotypes with LDL (p LT 0.05), LDL/HDL ratio (p LT 0.001), apoB (p LT 0.01), body weight (p LT 0.001) and waist circumference (p LT 0.001). Conclusion: Our findings indicate that there is an association between LEP G-2548A polymorphism and metabolic and anthropometric parameters in obese patients in a Serbian population.
T2  - Clinical Lipidology
T1  - Association of leptin gene polymorphism G-2548A with metabolic and anthropometric parameters in obese patients in a Serbian population: pilot study
VL  - 9
IS  - 5
SP  - 505
EP  - 513
DO  - 10.2217/CLP.14.42
ER  - 

@article{
author = "Soskić, Sanja S. and Stokić, Edita and Obradović, Milan M. and Sudar, Emina and Tanić, Nasta and Kupusinac, Aleksandar and Đorđević, Jelena D. and Isenović, Esma R.",
year = "2014",
abstract = "Aim: The aim of this pilot study was to investigate possible associations of LEP promoter polymorphism LEP G-2548A and obesity-associated metabolic and antropometric parameters in obese population. Materials and methods: Group of 31 patients with hyperalimentary type of obesity (mean age: 39.26 +/- 11.45 years; BMI: 41.51 +/- 9.22 kg/m(2)) and 36 healthy, nonobese, normal weight subjects (mean age: 33.55 +/- 6.46 years; BMI: 22.63 +/- 1.94 kg/m(2)) were studied. Blood samples were collected for DNA isolation, serum leptin and serum lipids measurements. LEP G-2548A genotypes were determined by PCR restriction fragment length polymorphism based analyses. Results: No significant differences in genotype and allele frequencies of the LEP G-2548A polymorphism were detected between obese and normal weight subjects. No association was found between this polymorphism and BMI. Obese subjects had statistically significant increase in serum leptin levels compared with control, while no association between leptin concentration and LEP polymorphism LEP G-2548A was found. There is a statistically significant association of LEP G-2548A genotypes with LDL (p LT 0.05), LDL/HDL ratio (p LT 0.001), apoB (p LT 0.01), body weight (p LT 0.001) and waist circumference (p LT 0.001). Conclusion: Our findings indicate that there is an association between LEP G-2548A polymorphism and metabolic and anthropometric parameters in obese patients in a Serbian population.",
journal = "Clinical Lipidology",
title = "Association of leptin gene polymorphism G-2548A with metabolic and anthropometric parameters in obese patients in a Serbian population: pilot study",
volume = "9",
number = "5",
pages = "505-513",
doi = "10.2217/CLP.14.42"
}

Soskić, S. S., Stokić, E., Obradović, M. M., Sudar, E., Tanić, N., Kupusinac, A., Đorđević, J. D.,& Isenović, E. R.. (2014). Association of leptin gene polymorphism G-2548A with metabolic and anthropometric parameters in obese patients in a Serbian population: pilot study. in Clinical Lipidology, 9(5), 505-513.
https://doi.org/10.2217/CLP.14.42

Soskić SS, Stokić E, Obradović MM, Sudar E, Tanić N, Kupusinac A, Đorđević JD, Isenović ER. Association of leptin gene polymorphism G-2548A with metabolic and anthropometric parameters in obese patients in a Serbian population: pilot study. in Clinical Lipidology. 2014;9(5):505-513.
doi:10.2217/CLP.14.42 .

Soskić, Sanja S., Stokić, Edita, Obradović, Milan M., Sudar, Emina, Tanić, Nasta, Kupusinac, Aleksandar, Đorđević, Jelena D., Isenović, Esma R., "Association of leptin gene polymorphism G-2548A with metabolic and anthropometric parameters in obese patients in a Serbian population: pilot study" in Clinical Lipidology, 9, no. 5 (2014):505-513,
https://doi.org/10.2217/CLP.14.42 . .

TY  - JOUR
AU  - Soskić, Sanja S.
AU  - Stokić, Edita
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/6013
AB  - Currently, vitamin D deficiency and obesity are pandemic diseases and they are associated with cardiovascular (CV) disease, metabolic syndrome and type 2 diabetes mellitus (T2DM) and other diseases. Concentrations of 25-hydroxyvitamin D (25(OH) D) (25D) are considered as the best indicator of total body vitamin D stores. An association between reduced circulating 25D concentrations and obesity is well known, but the mechanisms are not totally clear. The role of vitamin D supplementation is still uncertain and prospective interventions will establish its influence, if any, in the treatment of obesity. Vitamin D deficiency is associated with the presence of a cardiometabolic risk profile in the obese. Future trials may establish a role for Vitamin D supplementation in individuals at increased CV risk.
T2  - Current Medical Research and Opinion
T1  - The relationship between vitamin D and obesity
VL  - 30
IS  - 6
SP  - 1197
EP  - 1199
DO  - 10.1185/03007995.2014.900004
ER  - 

@article{
author = "Soskić, Sanja S. and Stokić, Edita and Isenović, Esma R.",
year = "2014",
abstract = "Currently, vitamin D deficiency and obesity are pandemic diseases and they are associated with cardiovascular (CV) disease, metabolic syndrome and type 2 diabetes mellitus (T2DM) and other diseases. Concentrations of 25-hydroxyvitamin D (25(OH) D) (25D) are considered as the best indicator of total body vitamin D stores. An association between reduced circulating 25D concentrations and obesity is well known, but the mechanisms are not totally clear. The role of vitamin D supplementation is still uncertain and prospective interventions will establish its influence, if any, in the treatment of obesity. Vitamin D deficiency is associated with the presence of a cardiometabolic risk profile in the obese. Future trials may establish a role for Vitamin D supplementation in individuals at increased CV risk.",
journal = "Current Medical Research and Opinion",
title = "The relationship between vitamin D and obesity",
volume = "30",
number = "6",
pages = "1197-1199",
doi = "10.1185/03007995.2014.900004"
}

Soskić, S. S., Stokić, E.,& Isenović, E. R.. (2014). The relationship between vitamin D and obesity. in Current Medical Research and Opinion, 30(6), 1197-1199.
https://doi.org/10.1185/03007995.2014.900004

Soskić SS, Stokić E, Isenović ER. The relationship between vitamin D and obesity. in Current Medical Research and Opinion. 2014;30(6):1197-1199.
doi:10.1185/03007995.2014.900004 .

Soskić, Sanja S., Stokić, Edita, Isenović, Esma R., "The relationship between vitamin D and obesity" in Current Medical Research and Opinion, 30, no. 6 (2014):1197-1199,
https://doi.org/10.1185/03007995.2014.900004 . .

TY  - JOUR
AU  - Rizzo, Manfredi
AU  - Rizvi, Ali A.
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Obradović, Milan M.
AU  - Montalto, Giuseppe
AU  - Boutjdir, Mohamed
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5565
AB  - Ghrelin is a peptide hormone produced mainly in the stomach that has widespread tissue distribution and diverse hormonal, metabolic and cardiovascular activities. The circulating ghrelin concentration increases during fasting and decreases after food intake. Ghrelin secretion may thus be initiated by food intake and is possibly controlled by nutritional factors. Lean subjects have increased levels of circulating ghrelin compared with obese subjects. Recent reports show that low plasma ghrelin is associated with elevated fasting insulin levels, insulin resistance and type 2 diabetes mellitus. Factors involved in the regulation of ghrelin secretion have not yet been defined; however, it is assumed that blood glucose levels represent a significant regulator. Recent evidence indicates that ghrelin can increase myocardial contractility, enhance vasodilatation, and has protective effect from myocardial damage. It has been shown that ghrelin may improve cardiac function through growth hormone (GH)-dependent mechanisms but there is also evidence to suggest that ghrelins cardioprotective activity is independent of GH. Recent data demonstrate that ghrelin can influence key events in atherogenesis. Thus, ghrelin may be a new target for the treatment of some cardiovascular diseases. In this review, we consider the current literature focusing on ghrelin as a potential antiatherogenic agent in the treatment of various pathophysiological conditions.
T2  - Current Pharmaceutical Design
T1  - A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin
VL  - 19
IS  - 27
SP  - 4953
EP  - 4963
DO  - 10.2174/1381612811319270018
ER  - 

@article{
author = "Rizzo, Manfredi and Rizvi, Ali A. and Sudar, Emina and Soskić, Sanja S. and Obradović, Milan M. and Montalto, Giuseppe and Boutjdir, Mohamed and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2013",
abstract = "Ghrelin is a peptide hormone produced mainly in the stomach that has widespread tissue distribution and diverse hormonal, metabolic and cardiovascular activities. The circulating ghrelin concentration increases during fasting and decreases after food intake. Ghrelin secretion may thus be initiated by food intake and is possibly controlled by nutritional factors. Lean subjects have increased levels of circulating ghrelin compared with obese subjects. Recent reports show that low plasma ghrelin is associated with elevated fasting insulin levels, insulin resistance and type 2 diabetes mellitus. Factors involved in the regulation of ghrelin secretion have not yet been defined; however, it is assumed that blood glucose levels represent a significant regulator. Recent evidence indicates that ghrelin can increase myocardial contractility, enhance vasodilatation, and has protective effect from myocardial damage. It has been shown that ghrelin may improve cardiac function through growth hormone (GH)-dependent mechanisms but there is also evidence to suggest that ghrelins cardioprotective activity is independent of GH. Recent data demonstrate that ghrelin can influence key events in atherogenesis. Thus, ghrelin may be a new target for the treatment of some cardiovascular diseases. In this review, we consider the current literature focusing on ghrelin as a potential antiatherogenic agent in the treatment of various pathophysiological conditions.",
journal = "Current Pharmaceutical Design",
title = "A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin",
volume = "19",
number = "27",
pages = "4953-4963",
doi = "10.2174/1381612811319270018"
}

Rizzo, M., Rizvi, A. A., Sudar, E., Soskić, S. S., Obradović, M. M., Montalto, G., Boutjdir, M., Mikhailidis, D. P.,& Isenović, E. R.. (2013). A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin. in Current Pharmaceutical Design, 19(27), 4953-4963.
https://doi.org/10.2174/1381612811319270018

Rizzo M, Rizvi AA, Sudar E, Soskić SS, Obradović MM, Montalto G, Boutjdir M, Mikhailidis DP, Isenović ER. A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin. in Current Pharmaceutical Design. 2013;19(27):4953-4963.
doi:10.2174/1381612811319270018 .

Rizzo, Manfredi, Rizvi, Ali A., Sudar, Emina, Soskić, Sanja S., Obradović, Milan M., Montalto, Giuseppe, Boutjdir, Mohamed, Mikhailidis, Dimitri P., Isenović, Esma R., "A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin" in Current Pharmaceutical Design, 19, no. 27 (2013):4953-4963,
https://doi.org/10.2174/1381612811319270018 . .

TY  - CHAP
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Zarić, Božidarka
AU  - Rašić-Milutinović, Zorica
AU  - Smiljanić, Katarina
AU  - Radak, Đorđe J.
AU  - Mikhailidis, Dimitri P.
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8685
AB  - Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.
T2  - Ghrelin: Production, Action Mechanisms and Physiological Effects
T1  - Ghrelin, obesity and atherosclerosis
SP  - 111
EP  - 126
UR  - https://hdl.handle.net/21.15107/rcub_vinar_8685
ER  - 

@inbook{
author = "Sudar, Emina and Soskić, Sanja S. and Zarić, Božidarka and Rašić-Milutinović, Zorica and Smiljanić, Katarina and Radak, Đorđe J. and Mikhailidis, Dimitri P. and Rizzo, Manfredi and Isenović, Esma R.",
year = "2012",
abstract = "Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.",
journal = "Ghrelin: Production, Action Mechanisms and Physiological Effects",
booktitle = "Ghrelin, obesity and atherosclerosis",
pages = "111-126",
url = "https://hdl.handle.net/21.15107/rcub_vinar_8685"
}

Sudar, E., Soskić, S. S., Zarić, B., Rašić-Milutinović, Z., Smiljanić, K., Radak, Đ. J., Mikhailidis, D. P., Rizzo, M.,& Isenović, E. R.. (2012). Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects, 111-126.
https://hdl.handle.net/21.15107/rcub_vinar_8685

Sudar E, Soskić SS, Zarić B, Rašić-Milutinović Z, Smiljanić K, Radak ĐJ, Mikhailidis DP, Rizzo M, Isenović ER. Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects. 2012;:111-126.
https://hdl.handle.net/21.15107/rcub_vinar_8685 .

Sudar, Emina, Soskić, Sanja S., Zarić, Božidarka, Rašić-Milutinović, Zorica, Smiljanić, Katarina, Radak, Đorđe J., Mikhailidis, Dimitri P., Rizzo, Manfredi, Isenović, Esma R., "Ghrelin, obesity and atherosclerosis" in Ghrelin: Production, Action Mechanisms and Physiological Effects (2012):111-126,
https://hdl.handle.net/21.15107/rcub_vinar_8685 .

TY  - JOUR
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Obradović, Milan M.
AU  - Nikolić, Dragana
AU  - Gluvić, Zoran
AU  - Stokić, Edita
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10323
AB  - Gojaznost se danas smatra bolešću savremenog društva i njena zastupljenost u svetu ima karakter epidemije. Istraživanja usmerena na razumevanje biologije adipocitne ćelije i adipoznog tkiva, značajno doprinose rasvetljavanju mnogih aspekata različitih metaboličkih poremećaja koji prate pojavu gojaznosti tj. prekomerenog prisustva adipoznog tkiva. Gojaznost je posledica dugotrajnog pozitivnog energetskog balansa, neprimerenog stilu života savremenog čoveka. Danas je utemeljena činjenica da je adipozno tkivo endokrini organ u kojem se sintetiše i eksprimira više od 60 različitih faktora - adipokina, sa snažnim uticajem na veliki broj metaboličkih procesa u organizmu. Adipokini mogu imati pro-inflamatorno ili anti-inflamatorno dejstvo. Mnogobrojna istraživanja jasno ukazuju na uzročnu vezu gojaznosti i hronične inflamacije slabog inteziteta, koja vodi razvoju poremećaja vezanih za prisustvo gojaznosti, naročito metaboličkih poremećaja koji znatno umanjuju kvalitet života. Svojom endokrinom funkcijom, adipocitne ćelije reflektuju metabolički status i prenose informaciju na druge organe, tkiva kao i centralni nervni sistem.
AB  - Obesity is a disease of the modern society and considering the number of obese people it has character of the worldwide epidemic. Understanding the biology of adipocytes and the events occurring in adipose tissue contributes to clarification of many aspects of the various metabolic disorders associated with obesity and excessive presence of adipose tissue. Overweight in individuals is the result of a long-term positive energy balance inappropriate to life style of the modern man. Today, it is well accepted that adipose tissue is an endocrine organ in which more than 60 of adipokines are synthesized and are expressed with strong influence on a great number of metabolic processes in organism. Adipokines have pro-inflammatory or anti-inflammatory effects. Increasing evidence indicates that obesity is causally linked to a chronic low-grade inflammatory state, and contributes to the development of obesity-linked disorders, in particular to metabolic dysfunction which significantly reduces the quality of life. Adipocytes, with their endocrine function, reflect metabolic status and transport information into organs, tissues and central nervous system, too.
T2  - Medicinska istraživanja
T1  - Patofiziologija gojaznosti
T1  - Pathophysiology of obesity
VL  - 46
IS  - 1
SP  - 43
EP  - 54
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10323
ER  - 

@article{
author = "Dobutović, Branislava and Sudar, Emina and Soskić, Sanja S. and Obradović, Milan M. and Nikolić, Dragana and Gluvić, Zoran and Stokić, Edita and Radak, Đorđe J. and Isenović, Esma R.",
year = "2012",
abstract = "Gojaznost se danas smatra bolešću savremenog društva i njena zastupljenost u svetu ima karakter epidemije. Istraživanja usmerena na razumevanje biologije adipocitne ćelije i adipoznog tkiva, značajno doprinose rasvetljavanju mnogih aspekata različitih metaboličkih poremećaja koji prate pojavu gojaznosti tj. prekomerenog prisustva adipoznog tkiva. Gojaznost je posledica dugotrajnog pozitivnog energetskog balansa, neprimerenog stilu života savremenog čoveka. Danas je utemeljena činjenica da je adipozno tkivo endokrini organ u kojem se sintetiše i eksprimira više od 60 različitih faktora - adipokina, sa snažnim uticajem na veliki broj metaboličkih procesa u organizmu. Adipokini mogu imati pro-inflamatorno ili anti-inflamatorno dejstvo. Mnogobrojna istraživanja jasno ukazuju na uzročnu vezu gojaznosti i hronične inflamacije slabog inteziteta, koja vodi razvoju poremećaja vezanih za prisustvo gojaznosti, naročito metaboličkih poremećaja koji znatno umanjuju kvalitet života. Svojom endokrinom funkcijom, adipocitne ćelije reflektuju metabolički status i prenose informaciju na druge organe, tkiva kao i centralni nervni sistem., Obesity is a disease of the modern society and considering the number of obese people it has character of the worldwide epidemic. Understanding the biology of adipocytes and the events occurring in adipose tissue contributes to clarification of many aspects of the various metabolic disorders associated with obesity and excessive presence of adipose tissue. Overweight in individuals is the result of a long-term positive energy balance inappropriate to life style of the modern man. Today, it is well accepted that adipose tissue is an endocrine organ in which more than 60 of adipokines are synthesized and are expressed with strong influence on a great number of metabolic processes in organism. Adipokines have pro-inflammatory or anti-inflammatory effects. Increasing evidence indicates that obesity is causally linked to a chronic low-grade inflammatory state, and contributes to the development of obesity-linked disorders, in particular to metabolic dysfunction which significantly reduces the quality of life. Adipocytes, with their endocrine function, reflect metabolic status and transport information into organs, tissues and central nervous system, too.",
journal = "Medicinska istraživanja",
title = "Patofiziologija gojaznosti, Pathophysiology of obesity",
volume = "46",
number = "1",
pages = "43-54",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10323"
}

Dobutović, B., Sudar, E., Soskić, S. S., Obradović, M. M., Nikolić, D., Gluvić, Z., Stokić, E., Radak, Đ. J.,& Isenović, E. R.. (2012). Patofiziologija gojaznosti. in Medicinska istraživanja, 46(1), 43-54.
https://hdl.handle.net/21.15107/rcub_vinar_10323

Dobutović B, Sudar E, Soskić SS, Obradović MM, Nikolić D, Gluvić Z, Stokić E, Radak ĐJ, Isenović ER. Patofiziologija gojaznosti. in Medicinska istraživanja. 2012;46(1):43-54.
https://hdl.handle.net/21.15107/rcub_vinar_10323 .

Dobutović, Branislava, Sudar, Emina, Soskić, Sanja S., Obradović, Milan M., Nikolić, Dragana, Gluvić, Zoran, Stokić, Edita, Radak, Đorđe J., Isenović, Esma R., "Patofiziologija gojaznosti" in Medicinska istraživanja, 46, no. 1 (2012):43-54,
https://hdl.handle.net/21.15107/rcub_vinar_10323 .

TY  - JOUR
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Obradović, Milan M.
AU  - Soskić, Sanja S.
AU  - Jovanović, Aleksandra
AU  - Stokić, Edita
AU  - Gluvić, Zoran
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10322
AB  - Gojaznost se definiše kao prekomerno prisustvo masnog tkiva u organizmu koje može dovesti do mnogih zdravstvenih komplikacija koje pogoršavaju kvalitet života i skraćuju životni vek. Gojaznost je rezultat fizioloških odgovora organizma u situaciji kada je kalorijski unos veći od stvarnih energetskih potreba organizma u dužem vremenskom periodu, bez adekvatnog utroška energije. Prema podacima Svetske zdravstvene organizacije (WHO) gojaznost zauzima peto mesto u paleti vodećih uzroka smrti na globalnom nivou i može se definisati kao hroničan poremećaj metabolizma koji je udružen sa kardiovaskularnim oboljenjima (CVD) kao i sa povećanom stopom morbiditeta i mortaliteta. Danas je prihvaćeno mišljenje da je gojaznost usko povezana sa razvojem rezistencije na insulin (IR). Metaboličke i hormonske promene, koje su posledica pre svega visceralne gojaznosti karakteristične za metabolički sindrom, dovode vremenom do pojave IR u adipoznom tkivu, jetri i mišićnom tkivu. Pretpostavlja se da IR koja se javlja usled gojaznosti predstavlja prvi korak u razvoju CVD. Delimično, IR povećava rizik za nastanak nekih CVD zbog hipertenzije i dislipidemije, kao i promena u adipocitokinima, koje vode inflamaciji krvnih sudova. Osim toga, gojaznost nepovoljno utiče kako na hemodinamiku, tako i na strukturu i funkciju kardiovaskularnog sistema (CVS). Kardiovaskularne komplikacije koje su povezane sa gojaznošću doprinose visokoj stopi morbiditeta i mortaliteta. Usled porasta broja gojaznih osoba, kao i prisustva IR i CVD kod ovih osoba, izučavanje masnog tkiva i njegovog uticaja na razvoj različitih patofizioloških stanja kao što su IR i CVD predstavljaju veoma važno polje biomedicinskih istraživanja, rezultati kojih bi zasigurno omogućili nove terapeutske pristupe u lečenju ovih poremećaja. Takođe, u cilju sprečavanja razvoja gojaznosti, a samim tim i oboljenja koja nastaju kao posledica ovog poremećaja, veoma veliki značaj imaju prevencija i edukacija o mogućim aspektima koje prekomerna akumulacija masnog tkiva može imati na normalno funkcionisanje organizma.
AB  - Obesity is defined as abnormal or excessive fat tissue accumulation that may impair health and well-being and also increases death risk. Obesity occurs as a result of physiological responses of the organism in situations when the caloric intake is greater than energy expenditure/ consumption over an extended period of time, resulting in energy conservation. According to the World Health Organization (WHO) overweight and obesity are the fifth of the leading risk factors for global deaths and they could be defined as a chronic metabolic disorder associated with cardiovascular diseases (CVD) and increased risk of morbidity and mortality. Today, it is accepted that obesity is closely related to insulin resistance (IR). Metabolic and hormonal changes occurring first of all with increased visceral obesity which is a characteristic of metabolic syndrome, lead to IR development in adipose, liver and muscle tissue. It is assumed that IR, which occurs due to obesity, represents the first step in CVD development. Partly, IR increases the risk for CVD development due to the presence of multiple risk factors as hypertension and dyslipidemia, and changes in adipocytokines lead to blood vessel inflammation. Besides that, obesity adversely affects hemodynamic, structure and function of cardiovascular system (CVS). Cardiovascular complications associated with obesity greatly contribute to increased risk of morbidity and mortality. Due to the rising number of obese patients and also presence of IR and CVD in these patients, the study of adipose tissue and its effects on the development of various pathophysiological states as IR and CVD represents a very important area of biomedical research which would lead to new therapeutic approaches in these conditions. Also, in order to prevent obesity development and associated disorders, prevention and education are of great importance.
T2  - Medicinska istraživanja
T1  - Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja
T1  - Obesity, insulin resistance and cardiovascular disease
VL  - 46
IS  - 2
SP  - 54
EP  - 59
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10322
ER  - 

@article{
author = "Sudar, Emina and Zafirović, Sonja and Obradović, Milan M. and Soskić, Sanja S. and Jovanović, Aleksandra and Stokić, Edita and Gluvić, Zoran and Isenović, Esma R.",
year = "2012",
abstract = "Gojaznost se definiše kao prekomerno prisustvo masnog tkiva u organizmu koje može dovesti do mnogih zdravstvenih komplikacija koje pogoršavaju kvalitet života i skraćuju životni vek. Gojaznost je rezultat fizioloških odgovora organizma u situaciji kada je kalorijski unos veći od stvarnih energetskih potreba organizma u dužem vremenskom periodu, bez adekvatnog utroška energije. Prema podacima Svetske zdravstvene organizacije (WHO) gojaznost zauzima peto mesto u paleti vodećih uzroka smrti na globalnom nivou i može se definisati kao hroničan poremećaj metabolizma koji je udružen sa kardiovaskularnim oboljenjima (CVD) kao i sa povećanom stopom morbiditeta i mortaliteta. Danas je prihvaćeno mišljenje da je gojaznost usko povezana sa razvojem rezistencije na insulin (IR). Metaboličke i hormonske promene, koje su posledica pre svega visceralne gojaznosti karakteristične za metabolički sindrom, dovode vremenom do pojave IR u adipoznom tkivu, jetri i mišićnom tkivu. Pretpostavlja se da IR koja se javlja usled gojaznosti predstavlja prvi korak u razvoju CVD. Delimično, IR povećava rizik za nastanak nekih CVD zbog hipertenzije i dislipidemije, kao i promena u adipocitokinima, koje vode inflamaciji krvnih sudova. Osim toga, gojaznost nepovoljno utiče kako na hemodinamiku, tako i na strukturu i funkciju kardiovaskularnog sistema (CVS). Kardiovaskularne komplikacije koje su povezane sa gojaznošću doprinose visokoj stopi morbiditeta i mortaliteta. Usled porasta broja gojaznih osoba, kao i prisustva IR i CVD kod ovih osoba, izučavanje masnog tkiva i njegovog uticaja na razvoj različitih patofizioloških stanja kao što su IR i CVD predstavljaju veoma važno polje biomedicinskih istraživanja, rezultati kojih bi zasigurno omogućili nove terapeutske pristupe u lečenju ovih poremećaja. Takođe, u cilju sprečavanja razvoja gojaznosti, a samim tim i oboljenja koja nastaju kao posledica ovog poremećaja, veoma veliki značaj imaju prevencija i edukacija o mogućim aspektima koje prekomerna akumulacija masnog tkiva može imati na normalno funkcionisanje organizma., Obesity is defined as abnormal or excessive fat tissue accumulation that may impair health and well-being and also increases death risk. Obesity occurs as a result of physiological responses of the organism in situations when the caloric intake is greater than energy expenditure/ consumption over an extended period of time, resulting in energy conservation. According to the World Health Organization (WHO) overweight and obesity are the fifth of the leading risk factors for global deaths and they could be defined as a chronic metabolic disorder associated with cardiovascular diseases (CVD) and increased risk of morbidity and mortality. Today, it is accepted that obesity is closely related to insulin resistance (IR). Metabolic and hormonal changes occurring first of all with increased visceral obesity which is a characteristic of metabolic syndrome, lead to IR development in adipose, liver and muscle tissue. It is assumed that IR, which occurs due to obesity, represents the first step in CVD development. Partly, IR increases the risk for CVD development due to the presence of multiple risk factors as hypertension and dyslipidemia, and changes in adipocytokines lead to blood vessel inflammation. Besides that, obesity adversely affects hemodynamic, structure and function of cardiovascular system (CVS). Cardiovascular complications associated with obesity greatly contribute to increased risk of morbidity and mortality. Due to the rising number of obese patients and also presence of IR and CVD in these patients, the study of adipose tissue and its effects on the development of various pathophysiological states as IR and CVD represents a very important area of biomedical research which would lead to new therapeutic approaches in these conditions. Also, in order to prevent obesity development and associated disorders, prevention and education are of great importance.",
journal = "Medicinska istraživanja",
title = "Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja, Obesity, insulin resistance and cardiovascular disease",
volume = "46",
number = "2",
pages = "54-59",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10322"
}

Sudar, E., Zafirović, S., Obradović, M. M., Soskić, S. S., Jovanović, A., Stokić, E., Gluvić, Z.,& Isenović, E. R.. (2012). Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja. in Medicinska istraživanja, 46(2), 54-59.
https://hdl.handle.net/21.15107/rcub_vinar_10322

Sudar E, Zafirović S, Obradović MM, Soskić SS, Jovanović A, Stokić E, Gluvić Z, Isenović ER. Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja. in Medicinska istraživanja. 2012;46(2):54-59.
https://hdl.handle.net/21.15107/rcub_vinar_10322 .

Sudar, Emina, Zafirović, Sonja, Obradović, Milan M., Soskić, Sanja S., Jovanović, Aleksandra, Stokić, Edita, Gluvić, Zoran, Isenović, Esma R., "Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja" in Medicinska istraživanja, 46, no. 2 (2012):54-59,
https://hdl.handle.net/21.15107/rcub_vinar_10322 .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Nikolić, Dragana
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Tanasković, Slobodan
AU  - Boljević, Miljana
AU  - Mušicki, Biljana
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10325
AB  - Ateroskleroza se manifestuje kao bolest koronarnih, perifernih i cerebrovaskularnih arterija. Aterosklerotične promene dovode do sužavanja prečnika arterija što dovodi do ishemije u mnogobrojnim organima, čime je poremećeno normalno funkcionisanje kako organa tako i organizma u celini. Centralnu ulogu u patogenezi ateroskleroze zauzima aterogena dislipidemija. Razvoj ateroskleroze počinje malim oštećenjima endotela izazvanim različitim činiocima, koji mogu uticati na povećanje ekspresije adhezivnih molekula. Disfunkcionalni endotel je mesto gde dolazi do infiltracije i akumulacije lipoproteina male gustine (LDL) u vaskularnom zidu. LDL tada podleže oksidativnoj modifikaciji, a kao krajnji produkt nastaje oksidovani LDL (oxLDL). Mnogobrojna eksperimentalna istraživanja ukazuju da su male guste LDL-čestice mnogo aterogenije u poređenju sa većim i lakšim LDL česticama. LDL podleže različitom stepenu oksidacije. Minimalno oksidovani LDL (LDL( - )) pokazuje svoj aterogeni potencijal time što stimuliše vaskularne endotelne ćelije na lučenje velikog broja proinflamatornih molekula kao što su adhezivni molekuli, hemotaktni proteini i faktori rasta. Za razliku od LDL(-), potpuno oksidovani LDL nema sposobnost preuzimanja putem LDL receptora već ga prepoznaju recptori 'hvatači', što dovodi do formiranja makrofag penastih ćelija a u nastavku i stvaranja ateroma. Prisustvo oxLDL u cirkulaciji kod ljudi predstavlja jedan od glavnih faktora rizika od kardiovaskularnih bolesti i ateroskleroze. Buduće studije imaju zadatak da izuče šta se dešava sa oxLDL- om in vivo, kao i da li je i u kojoj meri oksidacija LDL koja igra ključnu ulogu u nastanku penastih ćelija, značajna u kasnijim fazama stvaranja plaka.U okviru ovog preglednog člana, izloženi su najnoviji podaci iz litearture o uticaju oxLDL-a u patogenezi arteroskleroze.
AB  - Atherosclerosis is manifested as a disease of coronary, cerebrovascular and peripheral arteries. Atherosclerotic changes lead to narrowing of the diameter of the arteries leading to ischemia in various organs, which disturbes the normal functioning of both organs and organism as a whole. Atherogenic dyslipidemia has a central role in the pathogenesis of atherosclerosis. Development of atherosclerosis begins with endothelial damage caused by variety of factors, which may cause an increase in expression of adhesion molecules. Dysfunctional endothelium is the place where infiltration and accumulation of low density lipoprotein (LDL) in the vascular wall occurs. LDL undergoes oxidative modification and the final product produced is oxidized LDL (oxLDL). Numerous experimental studies sug- gest that small dense LDL particles are particularly atherogenic compared with larger and lighter LDL particles. LDL is subject to varying degrees of oxidation. Minimally oxidized LDL (LDL(- )) exhibits its atherogenic potential by stimulating vascular endothelial cells to secrete a large number of proinflammatory molecules, such as adhesion molecules, chemotactic proteins, and growth factors. Unlike the LDL(-), fully oxidized LDL cannot bind the LDL receptors, but is recognized by scavenger receptors, which leads to the formation of macrophage foam cells and eventually atheroma. The presence of oxLDL in the circulation in humans is a major risk factor for cardiovascular disease and atherosclerosis. Future studies are warranted to elucidate the role of oxLDL in vivo, and whether and to what extent oxidation of LDL, which plays a key role in the development of foam cells, is critical for later stages in creating the plaque. In this review article, we present current knowledge of the impact of oxLDL in the pathogenesis of arteriosclerosis.
T2  - Medicinska istraživanja
T1  - Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze
T1  - Aterosclerosis and effect of oxidation low density lipoprotein in patogenesis of aterosclerosis
VL  - 45
IS  - 4
SP  - 66
EP  - 71
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10325
ER  - 

@article{
author = "Obradović, Milan M. and Nikolić, Dragana and Dobutović, Branislava and Sudar, Emina and Soskić, Sanja S. and Tanasković, Slobodan and Boljević, Miljana and Mušicki, Biljana and Radak, Đorđe J. and Isenović, Esma R.",
year = "2011",
abstract = "Ateroskleroza se manifestuje kao bolest koronarnih, perifernih i cerebrovaskularnih arterija. Aterosklerotične promene dovode do sužavanja prečnika arterija što dovodi do ishemije u mnogobrojnim organima, čime je poremećeno normalno funkcionisanje kako organa tako i organizma u celini. Centralnu ulogu u patogenezi ateroskleroze zauzima aterogena dislipidemija. Razvoj ateroskleroze počinje malim oštećenjima endotela izazvanim različitim činiocima, koji mogu uticati na povećanje ekspresije adhezivnih molekula. Disfunkcionalni endotel je mesto gde dolazi do infiltracije i akumulacije lipoproteina male gustine (LDL) u vaskularnom zidu. LDL tada podleže oksidativnoj modifikaciji, a kao krajnji produkt nastaje oksidovani LDL (oxLDL). Mnogobrojna eksperimentalna istraživanja ukazuju da su male guste LDL-čestice mnogo aterogenije u poređenju sa većim i lakšim LDL česticama. LDL podleže različitom stepenu oksidacije. Minimalno oksidovani LDL (LDL( - )) pokazuje svoj aterogeni potencijal time što stimuliše vaskularne endotelne ćelije na lučenje velikog broja proinflamatornih molekula kao što su adhezivni molekuli, hemotaktni proteini i faktori rasta. Za razliku od LDL(-), potpuno oksidovani LDL nema sposobnost preuzimanja putem LDL receptora već ga prepoznaju recptori 'hvatači', što dovodi do formiranja makrofag penastih ćelija a u nastavku i stvaranja ateroma. Prisustvo oxLDL u cirkulaciji kod ljudi predstavlja jedan od glavnih faktora rizika od kardiovaskularnih bolesti i ateroskleroze. Buduće studije imaju zadatak da izuče šta se dešava sa oxLDL- om in vivo, kao i da li je i u kojoj meri oksidacija LDL koja igra ključnu ulogu u nastanku penastih ćelija, značajna u kasnijim fazama stvaranja plaka.U okviru ovog preglednog člana, izloženi su najnoviji podaci iz litearture o uticaju oxLDL-a u patogenezi arteroskleroze., Atherosclerosis is manifested as a disease of coronary, cerebrovascular and peripheral arteries. Atherosclerotic changes lead to narrowing of the diameter of the arteries leading to ischemia in various organs, which disturbes the normal functioning of both organs and organism as a whole. Atherogenic dyslipidemia has a central role in the pathogenesis of atherosclerosis. Development of atherosclerosis begins with endothelial damage caused by variety of factors, which may cause an increase in expression of adhesion molecules. Dysfunctional endothelium is the place where infiltration and accumulation of low density lipoprotein (LDL) in the vascular wall occurs. LDL undergoes oxidative modification and the final product produced is oxidized LDL (oxLDL). Numerous experimental studies sug- gest that small dense LDL particles are particularly atherogenic compared with larger and lighter LDL particles. LDL is subject to varying degrees of oxidation. Minimally oxidized LDL (LDL(- )) exhibits its atherogenic potential by stimulating vascular endothelial cells to secrete a large number of proinflammatory molecules, such as adhesion molecules, chemotactic proteins, and growth factors. Unlike the LDL(-), fully oxidized LDL cannot bind the LDL receptors, but is recognized by scavenger receptors, which leads to the formation of macrophage foam cells and eventually atheroma. The presence of oxLDL in the circulation in humans is a major risk factor for cardiovascular disease and atherosclerosis. Future studies are warranted to elucidate the role of oxLDL in vivo, and whether and to what extent oxidation of LDL, which plays a key role in the development of foam cells, is critical for later stages in creating the plaque. In this review article, we present current knowledge of the impact of oxLDL in the pathogenesis of arteriosclerosis.",
journal = "Medicinska istraživanja",
title = "Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze, Aterosclerosis and effect of oxidation low density lipoprotein in patogenesis of aterosclerosis",
volume = "45",
number = "4",
pages = "66-71",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10325"
}

Obradović, M. M., Nikolić, D., Dobutović, B., Sudar, E., Soskić, S. S., Tanasković, S., Boljević, M., Mušicki, B., Radak, Đ. J.,& Isenović, E. R.. (2011). Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze. in Medicinska istraživanja, 45(4), 66-71.
https://hdl.handle.net/21.15107/rcub_vinar_10325

Obradović MM, Nikolić D, Dobutović B, Sudar E, Soskić SS, Tanasković S, Boljević M, Mušicki B, Radak ĐJ, Isenović ER. Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze. in Medicinska istraživanja. 2011;45(4):66-71.
https://hdl.handle.net/21.15107/rcub_vinar_10325 .

Obradović, Milan M., Nikolić, Dragana, Dobutović, Branislava, Sudar, Emina, Soskić, Sanja S., Tanasković, Slobodan, Boljević, Miljana, Mušicki, Biljana, Radak, Đorđe J., Isenović, Esma R., "Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze" in Medicinska istraživanja, 45, no. 4 (2011):66-71,
https://hdl.handle.net/21.15107/rcub_vinar_10325 .

TY  - JOUR
AU  - Sudar, Emina
AU  - Stokić, Edita
AU  - Nikolić, Dragana
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Obradović, Milan M.
AU  - Tanasković, Slobodan
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10326
AB  - Sekretagozi hormona rasta (GHS) su sintetička jedinjenja koja su potentni stimulatori oslobađanja hormona rasta (GH) i deluju preko receptora spregnutog sa guanin nukleotid-vezujućim (G) proteinom, koji se naziva GHS-receptor (GHS-R). Metodom reverzne farmakologije identifikovan je i okarakterisan endogeni ligand za GHS-R tipa 1a (GHS-R1a), koji je nazvan grelin. Grelin je peptidni hormon građen od 28 aminokiselina, u kome je aminokiselina Serin-3 (Ser3) noktanoilovana, odnosno ima modifikaciju u vidu lanca masnih kiselina koja je esencijalna za njegovu aktivnost. Grelin se najviše sintetiše u želucu, a GHS-R su eksprimirani većinom u hipotalamusu i hipofizi. Ishrana je najvažniji faktor koji utiče na regulaciju sekrecije grelina. Koncentracija grelina u cirkulaciji povećana je za vreme gladovanja, a opada nakon uzimanja hrane. Grelin stimuliše oslobađanje GH u mnogo većim količinama nego maksimalne doze GH-oslobađajućeg hormona (GHRH) što ukazuje na drugačiji mehanizam delovanja grelina na nivou hipofize. iRNK za grelin i za GHS-R1a identifikovane su i u srcu i u aorti. Proučavanja efekata grelina, pokazala su njegove povoljne efekte na kardiovaskularni sistem (CVS). S obzirom da grelin stimuliše oslobađanje GH, za koji je ranije pokazano da ima kardioprotektivne efekte, grelin može da ispoljava povoljne efekte na CVS posredovane preko GH, ali i efekte koji su nezavisni od efekata GH. Povoljni efekti grelina na CVS pružaju mogućnost da se grelin koristi u terapiji oboljenja CVS kao što su poremećaji u radu srca, hipertenzija i bolesti ishemije srca.
AB  - Small synthetic molecules called growth hormone (GH) secretagogues (GHS) stimulate the release of GH from the pituitary. They act through the GHS-receptor (GHS-R), a G protein coupled receptor. Recently, by using a method of reverse pharmacology the endogenous ligand for the GHS-R type 1a (GHS-R1a) has been discovered. Ghrelin is a 28 amino acid peptide hormone in which the third amino acid serine (Ser3) is modified by a fatty acid and this modification is essential for ghrelin's activity. Ghrelin is produced mainly in the stomach and GHS-R is mainly expressed in hypothalamus and in the pituitary. The discovery of ghrelin indicates that the release of GH from the pituitary might be regulated not only by hypothalamic GH-releasing hormone (GHRH), but also by ghrelin derived from the stomach. In addition, ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, a region known to control food intake. The tissue distribution of ghrelin is widespread, and it is also present in cardiomyocytes. In addition, expression of mRNA encoding both ghrelin and GHSR-1a has been observed in the heart and aortas. Recent evidence indicates that ghrelin feature a variety of cardiovascular activities, including increase of myocardial contractility, vasodilatation, and protection from myocardial infarction. It has been shown that ghrelin may improve cardiac function partly through GH dependent mechanisms but also, some evidence suggests that ghrelin's cardioprotective activity is independent from GH secretion. Thus, ghrelin may be a new therapeutic agent for the treatment of some cardiovascular disturbances and diseases. Further studies are necessary to investigate the potential mechanisms for the effects of ghrelin on cardiovascular system.
T2  - Medicinska istraživanja
T1  - Opšte osobine i efekti grelina na kardiovaskularni sistem
T1  - Ghrelin structure and cardiovascular effects
VL  - 45
IS  - 4
SP  - 15
EP  - 29
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10326
ER  - 

@article{
author = "Sudar, Emina and Stokić, Edita and Nikolić, Dragana and Dobutović, Branislava and Soskić, Sanja S. and Obradović, Milan M. and Tanasković, Slobodan and Radak, Đorđe J. and Isenović, Esma R.",
year = "2011",
abstract = "Sekretagozi hormona rasta (GHS) su sintetička jedinjenja koja su potentni stimulatori oslobađanja hormona rasta (GH) i deluju preko receptora spregnutog sa guanin nukleotid-vezujućim (G) proteinom, koji se naziva GHS-receptor (GHS-R). Metodom reverzne farmakologije identifikovan je i okarakterisan endogeni ligand za GHS-R tipa 1a (GHS-R1a), koji je nazvan grelin. Grelin je peptidni hormon građen od 28 aminokiselina, u kome je aminokiselina Serin-3 (Ser3) noktanoilovana, odnosno ima modifikaciju u vidu lanca masnih kiselina koja je esencijalna za njegovu aktivnost. Grelin se najviše sintetiše u želucu, a GHS-R su eksprimirani većinom u hipotalamusu i hipofizi. Ishrana je najvažniji faktor koji utiče na regulaciju sekrecije grelina. Koncentracija grelina u cirkulaciji povećana je za vreme gladovanja, a opada nakon uzimanja hrane. Grelin stimuliše oslobađanje GH u mnogo većim količinama nego maksimalne doze GH-oslobađajućeg hormona (GHRH) što ukazuje na drugačiji mehanizam delovanja grelina na nivou hipofize. iRNK za grelin i za GHS-R1a identifikovane su i u srcu i u aorti. Proučavanja efekata grelina, pokazala su njegove povoljne efekte na kardiovaskularni sistem (CVS). S obzirom da grelin stimuliše oslobađanje GH, za koji je ranije pokazano da ima kardioprotektivne efekte, grelin može da ispoljava povoljne efekte na CVS posredovane preko GH, ali i efekte koji su nezavisni od efekata GH. Povoljni efekti grelina na CVS pružaju mogućnost da se grelin koristi u terapiji oboljenja CVS kao što su poremećaji u radu srca, hipertenzija i bolesti ishemije srca., Small synthetic molecules called growth hormone (GH) secretagogues (GHS) stimulate the release of GH from the pituitary. They act through the GHS-receptor (GHS-R), a G protein coupled receptor. Recently, by using a method of reverse pharmacology the endogenous ligand for the GHS-R type 1a (GHS-R1a) has been discovered. Ghrelin is a 28 amino acid peptide hormone in which the third amino acid serine (Ser3) is modified by a fatty acid and this modification is essential for ghrelin's activity. Ghrelin is produced mainly in the stomach and GHS-R is mainly expressed in hypothalamus and in the pituitary. The discovery of ghrelin indicates that the release of GH from the pituitary might be regulated not only by hypothalamic GH-releasing hormone (GHRH), but also by ghrelin derived from the stomach. In addition, ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, a region known to control food intake. The tissue distribution of ghrelin is widespread, and it is also present in cardiomyocytes. In addition, expression of mRNA encoding both ghrelin and GHSR-1a has been observed in the heart and aortas. Recent evidence indicates that ghrelin feature a variety of cardiovascular activities, including increase of myocardial contractility, vasodilatation, and protection from myocardial infarction. It has been shown that ghrelin may improve cardiac function partly through GH dependent mechanisms but also, some evidence suggests that ghrelin's cardioprotective activity is independent from GH secretion. Thus, ghrelin may be a new therapeutic agent for the treatment of some cardiovascular disturbances and diseases. Further studies are necessary to investigate the potential mechanisms for the effects of ghrelin on cardiovascular system.",
journal = "Medicinska istraživanja",
title = "Opšte osobine i efekti grelina na kardiovaskularni sistem, Ghrelin structure and cardiovascular effects",
volume = "45",
number = "4",
pages = "15-29",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10326"
}

Sudar, E., Stokić, E., Nikolić, D., Dobutović, B., Soskić, S. S., Obradović, M. M., Tanasković, S., Radak, Đ. J.,& Isenović, E. R.. (2011). Opšte osobine i efekti grelina na kardiovaskularni sistem. in Medicinska istraživanja, 45(4), 15-29.
https://hdl.handle.net/21.15107/rcub_vinar_10326

Sudar E, Stokić E, Nikolić D, Dobutović B, Soskić SS, Obradović MM, Tanasković S, Radak ĐJ, Isenović ER. Opšte osobine i efekti grelina na kardiovaskularni sistem. in Medicinska istraživanja. 2011;45(4):15-29.
https://hdl.handle.net/21.15107/rcub_vinar_10326 .

Sudar, Emina, Stokić, Edita, Nikolić, Dragana, Dobutović, Branislava, Soskić, Sanja S., Obradović, Milan M., Tanasković, Slobodan, Radak, Đorđe J., Isenović, Esma R., "Opšte osobine i efekti grelina na kardiovaskularni sistem" in Medicinska istraživanja, 45, no. 4 (2011):15-29,
https://hdl.handle.net/21.15107/rcub_vinar_10326 .

TY  - JOUR
AU  - Nikolić, Dragana
AU  - Gluvić, Zoran
AU  - Akšam, Slavica
AU  - Obradović, Milan M.
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Sudar, Emina
AU  - Trpković, Andreja
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10327
AB  - Oksidativni stres (OxS) je skup poremećaja dinamičke ravnoteže prooksidanasa i antioksidanasa koji nastaje usled povećane produkcije slobodnih radikala (SR) ili usled smanjene aktivnosti antioksidativnog zaštitnog sistema (AOS). Bolest koja se, takođe, povezuje sa OxS je i diabetes mellitus (DM). DM karakteriše povećani nivo glukoze u cirkulaciji, kao i drugi biohemijski poremećaji koji nastaju kao posledica neadekvatne produkcije ili neadekvatnog dejstva insulina. Dijabetes tipa 1 (DMT1) je prototip autoimune bolesti sa intenzivnim OxS. Antioksidativni enzim katalaza (CAT) smanjuje produkciju vodonik-peroksida koji može biti veoma toksičan za ćelije pankreasa. Povećanje aktivnosti CAT u svim fazama DMT1 indirektno potvrđuje značaj OxS u nastanku ove bolesti. Visoko reaktivni SR, nastali uglavnom zbog hiperglikemije, izazivaju OxS što dodatno ubrzava razvoj i napredovanje DM kao i njegovih komplikacija koje su uzrokovane redukovanom aktivnošću AOS. Uprkos brojnim dokazima o štetnim posledicama OxS u DM, veliki broj kliničkih ispitivanja sa klasičnim antioksidansima, nažalost, nije pokazao efikasnost njihove primene u lečenju DM. Novi terapijski pristup, koji uključuje primenu kako standardnih tako i novih antioksidanasa, se predlaže u algoritmima lečenja DM. Važno je ukazati na značaj doze primenjenih antioksidanasa, obzirom da je dokazano da pojedinačne visoke doze mogu delovati prooksidaciono. Takođe, važna je i dozna uravnoteženost primenjenih antioksidanasa i antidijabetika, u cilju efikasnijeg lečenja obolelih od DM. U okviru ovog rada fokusirali smo se na ulogu antioksidansa u lečenju DM.
AB  - Oxidative stress (OxS) represents an imbalance in dynamic equilibrium between prooxidants and antioxidants caused by increased free radical (FR) production or decreased activity of antioxidative system (AOS). OxS is involvedin many diseases such is diabetes mellitus (DM). DM presents with elevated blood glucose level and other biochemical disorders related to the inappropriate insulin secretion or improper insulin action. DM type 1 (DMT1) is an autoimmune disease with excessive OxS. The activity of antioxidative enzyme catalase (CAT) diminishes the production of hydrogen peroxide which is highly toxic for pancreatic cells. The increased activity of catalase (CAT) found in DMT1 patients signifies the importance of OxS in the pathogenesis of this disease. The generation of highly reactive FR, induced by hyperglycaemia, triggers the development of oxidative stress. Furthermore, OxS accelerates the development of DM and its complications which are related to the decreased activity of AOS. However, the standard antioxidant drugs failed in clinical trials for DM. New antioxidant agents combined with standard drugs are now proposed in therapy for DM. It is important to acknowledge that high doses of antioxidant agents could paradoxically have prooxidant effect. In addition, it is important to establish the dosage balance between antioxidant and antidiabetic drugs. In this article, we discuss the antioxidative agents and their significance in treatment of DM.
T2  - Medicinska istraživanja
T1  - Uloga antioksidanasa u lečenju diabetes mellitus-a
T1  - The role of antioxidative treatment in diabetes mellitus
VL  - 45
IS  - 2
SP  - 4
EP  - 12
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10327
ER  - 

@article{
author = "Nikolić, Dragana and Gluvić, Zoran and Akšam, Slavica and Obradović, Milan M. and Dobutović, Branislava and Soskić, Sanja S. and Sudar, Emina and Trpković, Andreja and Isenović, Esma R.",
year = "2011",
abstract = "Oksidativni stres (OxS) je skup poremećaja dinamičke ravnoteže prooksidanasa i antioksidanasa koji nastaje usled povećane produkcije slobodnih radikala (SR) ili usled smanjene aktivnosti antioksidativnog zaštitnog sistema (AOS). Bolest koja se, takođe, povezuje sa OxS je i diabetes mellitus (DM). DM karakteriše povećani nivo glukoze u cirkulaciji, kao i drugi biohemijski poremećaji koji nastaju kao posledica neadekvatne produkcije ili neadekvatnog dejstva insulina. Dijabetes tipa 1 (DMT1) je prototip autoimune bolesti sa intenzivnim OxS. Antioksidativni enzim katalaza (CAT) smanjuje produkciju vodonik-peroksida koji može biti veoma toksičan za ćelije pankreasa. Povećanje aktivnosti CAT u svim fazama DMT1 indirektno potvrđuje značaj OxS u nastanku ove bolesti. Visoko reaktivni SR, nastali uglavnom zbog hiperglikemije, izazivaju OxS što dodatno ubrzava razvoj i napredovanje DM kao i njegovih komplikacija koje su uzrokovane redukovanom aktivnošću AOS. Uprkos brojnim dokazima o štetnim posledicama OxS u DM, veliki broj kliničkih ispitivanja sa klasičnim antioksidansima, nažalost, nije pokazao efikasnost njihove primene u lečenju DM. Novi terapijski pristup, koji uključuje primenu kako standardnih tako i novih antioksidanasa, se predlaže u algoritmima lečenja DM. Važno je ukazati na značaj doze primenjenih antioksidanasa, obzirom da je dokazano da pojedinačne visoke doze mogu delovati prooksidaciono. Takođe, važna je i dozna uravnoteženost primenjenih antioksidanasa i antidijabetika, u cilju efikasnijeg lečenja obolelih od DM. U okviru ovog rada fokusirali smo se na ulogu antioksidansa u lečenju DM., Oxidative stress (OxS) represents an imbalance in dynamic equilibrium between prooxidants and antioxidants caused by increased free radical (FR) production or decreased activity of antioxidative system (AOS). OxS is involvedin many diseases such is diabetes mellitus (DM). DM presents with elevated blood glucose level and other biochemical disorders related to the inappropriate insulin secretion or improper insulin action. DM type 1 (DMT1) is an autoimmune disease with excessive OxS. The activity of antioxidative enzyme catalase (CAT) diminishes the production of hydrogen peroxide which is highly toxic for pancreatic cells. The increased activity of catalase (CAT) found in DMT1 patients signifies the importance of OxS in the pathogenesis of this disease. The generation of highly reactive FR, induced by hyperglycaemia, triggers the development of oxidative stress. Furthermore, OxS accelerates the development of DM and its complications which are related to the decreased activity of AOS. However, the standard antioxidant drugs failed in clinical trials for DM. New antioxidant agents combined with standard drugs are now proposed in therapy for DM. It is important to acknowledge that high doses of antioxidant agents could paradoxically have prooxidant effect. In addition, it is important to establish the dosage balance between antioxidant and antidiabetic drugs. In this article, we discuss the antioxidative agents and their significance in treatment of DM.",
journal = "Medicinska istraživanja",
title = "Uloga antioksidanasa u lečenju diabetes mellitus-a, The role of antioxidative treatment in diabetes mellitus",
volume = "45",
number = "2",
pages = "4-12",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10327"
}

Nikolić, D., Gluvić, Z., Akšam, S., Obradović, M. M., Dobutović, B., Soskić, S. S., Sudar, E., Trpković, A.,& Isenović, E. R.. (2011). Uloga antioksidanasa u lečenju diabetes mellitus-a. in Medicinska istraživanja, 45(2), 4-12.
https://hdl.handle.net/21.15107/rcub_vinar_10327

Nikolić D, Gluvić Z, Akšam S, Obradović MM, Dobutović B, Soskić SS, Sudar E, Trpković A, Isenović ER. Uloga antioksidanasa u lečenju diabetes mellitus-a. in Medicinska istraživanja. 2011;45(2):4-12.
https://hdl.handle.net/21.15107/rcub_vinar_10327 .

Nikolić, Dragana, Gluvić, Zoran, Akšam, Slavica, Obradović, Milan M., Dobutović, Branislava, Soskić, Sanja S., Sudar, Emina, Trpković, Andreja, Isenović, Esma R., "Uloga antioksidanasa u lečenju diabetes mellitus-a" in Medicinska istraživanja, 45, no. 2 (2011):4-12,
https://hdl.handle.net/21.15107/rcub_vinar_10327 .

TY  - JOUR
AU  - Soskić, Sanja S.
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Obradović, Milan M.
AU  - Nikolić, Dragana
AU  - Zarić, Božidarka
AU  - Stojanovic, Srdan D.
AU  - Stokić, Edita
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4519
AB  - The peroxisome proliferator-activated receptors (PPARs) represent the family of 3 nuclear receptor isoforms-PPAR alpha, -gamma, and -delta/beta, which are encoded by different genes. As lipid sensors, they are primarily involved in regulation of lipid metabolism and subsequently in inflammation and atherosclerosis. Atherosclerosis considers accumulation of the cells and extracellular matrix in the vessel wall leading to the formation of atherosclerotic plaque, atherothrombosis, and other vascular complications. Besides existence of natural ligands for PPARs, their more potent synthetic ligands are fibrates and thiazolidindiones. Future investigations should now focus on the mechanisms of PPARs activation, which might present new approaches involved in the antiatherosclerotic effects revealed in this review. In addition, in this review we are presenting latest data from recent performed clinical studies which have focus on novel approach to PPARs agonists as potential therapeutic agents in the treatment of complex disease such as atherosclerosis.
T2  - Angiology
T1  - Peroxisome Proliferator-Activated Receptors and Atherosclerosis
VL  - 62
IS  - 7
SP  - 523
EP  - 534
DO  - 10.1177/0003319711401012
ER  - 

@article{
author = "Soskić, Sanja S. and Dobutović, Branislava and Sudar, Emina and Obradović, Milan M. and Nikolić, Dragana and Zarić, Božidarka and Stojanovic, Srdan D. and Stokić, Edita and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2011",
abstract = "The peroxisome proliferator-activated receptors (PPARs) represent the family of 3 nuclear receptor isoforms-PPAR alpha, -gamma, and -delta/beta, which are encoded by different genes. As lipid sensors, they are primarily involved in regulation of lipid metabolism and subsequently in inflammation and atherosclerosis. Atherosclerosis considers accumulation of the cells and extracellular matrix in the vessel wall leading to the formation of atherosclerotic plaque, atherothrombosis, and other vascular complications. Besides existence of natural ligands for PPARs, their more potent synthetic ligands are fibrates and thiazolidindiones. Future investigations should now focus on the mechanisms of PPARs activation, which might present new approaches involved in the antiatherosclerotic effects revealed in this review. In addition, in this review we are presenting latest data from recent performed clinical studies which have focus on novel approach to PPARs agonists as potential therapeutic agents in the treatment of complex disease such as atherosclerosis.",
journal = "Angiology",
title = "Peroxisome Proliferator-Activated Receptors and Atherosclerosis",
volume = "62",
number = "7",
pages = "523-534",
doi = "10.1177/0003319711401012"
}

Soskić, S. S., Dobutović, B., Sudar, E., Obradović, M. M., Nikolić, D., Zarić, B., Stojanovic, S. D., Stokić, E., Mikhailidis, D. P.,& Isenović, E. R.. (2011). Peroxisome Proliferator-Activated Receptors and Atherosclerosis. in Angiology, 62(7), 523-534.
https://doi.org/10.1177/0003319711401012

Soskić SS, Dobutović B, Sudar E, Obradović MM, Nikolić D, Zarić B, Stojanovic SD, Stokić E, Mikhailidis DP, Isenović ER. Peroxisome Proliferator-Activated Receptors and Atherosclerosis. in Angiology. 2011;62(7):523-534.
doi:10.1177/0003319711401012 .

Soskić, Sanja S., Dobutović, Branislava, Sudar, Emina, Obradović, Milan M., Nikolić, Dragana, Zarić, Božidarka, Stojanovic, Srdan D., Stokić, Edita, Mikhailidis, Dimitri P., Isenović, Esma R., "Peroxisome Proliferator-Activated Receptors and Atherosclerosis" in Angiology, 62, no. 7 (2011):523-534,
https://doi.org/10.1177/0003319711401012 . .

TY  - JOUR
AU  - Sudar, Emina
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Mandušić, Vesna
AU  - Žakula, Zorica
AU  - Misirkić, Maja
AU  - Vucicevic, Ljubica
AU  - Janjetović, Kristina D.
AU  - Trajković, Vladimir S.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4317
AB  - The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.
T2  - Journal of Physiology and Biochemistry
T1  - Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats
VL  - 67
IS  - 2
SP  - 195
EP  - 204
DO  - 10.1007/s13105-010-0063-1
ER  - 

@article{
author = "Sudar, Emina and Dobutović, Branislava and Soskić, Sanja S. and Mandušić, Vesna and Žakula, Zorica and Misirkić, Maja and Vucicevic, Ljubica and Janjetović, Kristina D. and Trajković, Vladimir S. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2011",
abstract = "The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.",
journal = "Journal of Physiology and Biochemistry",
title = "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats",
volume = "67",
number = "2",
pages = "195-204",
doi = "10.1007/s13105-010-0063-1"
}

Sudar, E., Dobutović, B., Soskić, S. S., Mandušić, V., Žakula, Z., Misirkić, M., Vucicevic, L., Janjetović, K. D., Trajković, V. S., Mikhailidis, D. P.,& Isenović, E. R.. (2011). Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. in Journal of Physiology and Biochemistry, 67(2), 195-204.
https://doi.org/10.1007/s13105-010-0063-1

Sudar E, Dobutović B, Soskić SS, Mandušić V, Žakula Z, Misirkić M, Vucicevic L, Janjetović KD, Trajković VS, Mikhailidis DP, Isenović ER. Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. in Journal of Physiology and Biochemistry. 2011;67(2):195-204.
doi:10.1007/s13105-010-0063-1 .

Sudar, Emina, Dobutović, Branislava, Soskić, Sanja S., Mandušić, Vesna, Žakula, Zorica, Misirkić, Maja, Vucicevic, Ljubica, Janjetović, Kristina D., Trajković, Vladimir S., Mikhailidis, Dimitri P., Isenović, Esma R., "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats" in Journal of Physiology and Biochemistry, 67, no. 2 (2011):195-204,
https://doi.org/10.1007/s13105-010-0063-1 . .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Mikhailidis, Dimitri P.
AU  - Yassin, Hanaa Z.
AU  - Dobutović, Branislava
AU  - Smiljanić, Katarina
AU  - Soskić, Sanja S.
AU  - Mousa, Shaker A.
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4662
AB  - The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.
T2  - Current Pharmaceutical Design
T1  - Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome
VL  - 17
IS  - 33
SP  - 3699
EP  - 3712
DO  - 10.2174/138161211798220882
ER  - 

@article{
author = "Haidara, Mohamed A. and Mikhailidis, Dimitri P. and Yassin, Hanaa Z. and Dobutović, Branislava and Smiljanić, Katarina and Soskić, Sanja S. and Mousa, Shaker A. and Rizzo, Manfredi and Isenović, Esma R.",
year = "2011",
abstract = "The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.",
journal = "Current Pharmaceutical Design",
title = "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome",
volume = "17",
number = "33",
pages = "3699-3712",
doi = "10.2174/138161211798220882"
}

Haidara, M. A., Mikhailidis, D. P., Yassin, H. Z., Dobutović, B., Smiljanić, K., Soskić, S. S., Mousa, S. A., Rizzo, M.,& Isenović, E. R.. (2011). Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design, 17(33), 3699-3712.
https://doi.org/10.2174/138161211798220882

Haidara MA, Mikhailidis DP, Yassin HZ, Dobutović B, Smiljanić K, Soskić SS, Mousa SA, Rizzo M, Isenović ER. Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design. 2011;17(33):3699-3712.
doi:10.2174/138161211798220882 .

Haidara, Mohamed A., Mikhailidis, Dimitri P., Yassin, Hanaa Z., Dobutović, Branislava, Smiljanić, Katarina, Soskić, Sanja S., Mousa, Shaker A., Rizzo, Manfredi, Isenović, Esma R., "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome" in Current Pharmaceutical Design, 17, no. 33 (2011):3699-3712,
https://doi.org/10.2174/138161211798220882 . .