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  - JOUR
AU  - Panić, Anastasija
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Sudar-Milovanović, Emina
AU  - Petrović, Nina
AU  - Isenović, Esma R.
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8013
AB  - 17β-Estradiol (E2) is known to negatively regulate inducible nitric oxide (NO) synthase (iNOS) expression via estrogen receptor alpha (ER-α) activation in aortic vascular smooth muscle cells.Therefore, we sought to determine whether E2 can inhibit iNOS in vivo in hepatic tissue via the activation of ER-α and whether extracellular signal-regulated kinases 1/2 (ERK1/2)-miR-221 axis is involved in this process. Male Wistar rats were treated with a bolus injection of E2 intraperitoneally (40 μg/kg), and 24 hours after treatment the animals were sacrificed and the livers excised. The protein levels of iNOS, p50 and p65 subunits of nuclear factor κB (NFκB), ERα, ERK1/2 and protein kinase B (Akt), as well as the association of ERα/Src in liver lysates were assessed by Western blot. The expression of hepatic miR-221 was analyzed by qRT-PCR. Results show that E2 reduced hepatic iNOS protein expression (p less than 0.01), the protein level of ERα (p less than 0.05), ERK1/2 (p less than 0.05), Akt phosphorylation (p less than 0.001) and miR-221 expression (p less than 0.05). In contrast, hepatic ERα/Src kinase association level (p less than 0.05) increased after E2 treatment. Our results indicate that E2 inhibits hepatic iNOS via molecular mechanisms involving the activation of the ER-α and inhibition of ERK1/2-miR-221 axis.
T2  - Journal of biological regulators and homeostatic agents
T1  - 17β-estradiol inhibits hepatic iNOS via the activation of the estrogen receptor ER-α and inhibition of erk1/2-mir-221 axis
VL  - 32
IS  - 6
SP  - 1369
EP  - 1377
UR  - https://hdl.handle.net/21.15107/rcub_vinar_8013
ER  - 

@article{
author = "Panić, Anastasija and Stanimirović, Julijana and Obradović, Milan M. and Zafirović, Sonja and Sudar-Milovanović, Emina and Petrović, Nina and Isenović, Esma R.",
year = "2018",
abstract = "17β-Estradiol (E2) is known to negatively regulate inducible nitric oxide (NO) synthase (iNOS) expression via estrogen receptor alpha (ER-α) activation in aortic vascular smooth muscle cells.Therefore, we sought to determine whether E2 can inhibit iNOS in vivo in hepatic tissue via the activation of ER-α and whether extracellular signal-regulated kinases 1/2 (ERK1/2)-miR-221 axis is involved in this process. Male Wistar rats were treated with a bolus injection of E2 intraperitoneally (40 μg/kg), and 24 hours after treatment the animals were sacrificed and the livers excised. The protein levels of iNOS, p50 and p65 subunits of nuclear factor κB (NFκB), ERα, ERK1/2 and protein kinase B (Akt), as well as the association of ERα/Src in liver lysates were assessed by Western blot. The expression of hepatic miR-221 was analyzed by qRT-PCR. Results show that E2 reduced hepatic iNOS protein expression (p less than 0.01), the protein level of ERα (p less than 0.05), ERK1/2 (p less than 0.05), Akt phosphorylation (p less than 0.001) and miR-221 expression (p less than 0.05). In contrast, hepatic ERα/Src kinase association level (p less than 0.05) increased after E2 treatment. Our results indicate that E2 inhibits hepatic iNOS via molecular mechanisms involving the activation of the ER-α and inhibition of ERK1/2-miR-221 axis.",
journal = "Journal of biological regulators and homeostatic agents",
title = "17β-estradiol inhibits hepatic iNOS via the activation of the estrogen receptor ER-α and inhibition of erk1/2-mir-221 axis",
volume = "32",
number = "6",
pages = "1369-1377",
url = "https://hdl.handle.net/21.15107/rcub_vinar_8013"
}

Panić, A., Stanimirović, J., Obradović, M. M., Zafirović, S., Sudar-Milovanović, E., Petrović, N.,& Isenović, E. R.. (2018). 17β-estradiol inhibits hepatic iNOS via the activation of the estrogen receptor ER-α and inhibition of erk1/2-mir-221 axis. in Journal of biological regulators and homeostatic agents, 32(6), 1369-1377.
https://hdl.handle.net/21.15107/rcub_vinar_8013

Panić A, Stanimirović J, Obradović MM, Zafirović S, Sudar-Milovanović E, Petrović N, Isenović ER. 17β-estradiol inhibits hepatic iNOS via the activation of the estrogen receptor ER-α and inhibition of erk1/2-mir-221 axis. in Journal of biological regulators and homeostatic agents. 2018;32(6):1369-1377.
https://hdl.handle.net/21.15107/rcub_vinar_8013 .

Panić, Anastasija, Stanimirović, Julijana, Obradović, Milan M., Zafirović, Sonja, Sudar-Milovanović, Emina, Petrović, Nina, Isenović, Esma R., "17β-estradiol inhibits hepatic iNOS via the activation of the estrogen receptor ER-α and inhibition of erk1/2-mir-221 axis" in Journal of biological regulators and homeostatic agents, 32, no. 6 (2018):1369-1377,
https://hdl.handle.net/21.15107/rcub_vinar_8013 .

TY  - JOUR
AU  - Panić, Anastasija
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Perović, Milan
AU  - Lačković, Milena
AU  - Petrović, Nina
AU  - Isenović, Esma R.
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8399
AB  - Purpose: This study aimed to investigate in vivo effects of estradiol on the regulation of hepatic inducible nitric oxide synthase (iNOS) expression in the high fat (HF) diet-induced obesity. Also, we aimed to investigate whether activation of the extracellular signal-regulated kinase (ERK1/2), adenosine monophosphate-activated protein kinase (AMPK), Src kinase, and miR-221 is involved in estradiol-mediated regulation of iNOS in the liver of obese male Wistar rats. Male Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. Half of HF rats were treated with estradiol intraperitoneally (40 μg/kg), whereas the other half were placebo-treated 24 H before euthanasia. Results show that estradiol treatment of HF rats decreased hepatic iNOS mRNA (P < 0.05) and protein expression (P < 0.01), the protein levels of p65 subunit of nuclear factor κB (P < 0.05) and ERα (P < 0.05), ERK1/2 phosphorylation (P < 0.001), and ERα/Src kinase association (P < 0.05). By contrast, hepatic Src protein level (P < 0.05), AMPKα phosphorylation (P < 0.05), and miR-221 expression (P < 0.05) were increased in HF rats after estradiol treatment. Our results indicate that estradiol in vivo regulates hepatic iNOS expression in obese rats via molecular mechanisms involving ERK1/2, AMPK, Src, and miR-221 signaling. © 2018 International Union of Biochemistry and Molecular Biology, Inc.
T2  - Biotechnology and Applied Biochemistry
T1  - Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221
VL  - 65
IS  - 6
SP  - 797
EP  - 806
DO  - 10.1002/bab.1680
ER  - 

@article{
author = "Panić, Anastasija and Stanimirović, Julijana and Obradović, Milan M. and Sudar-Milovanović, Emina and Perović, Milan and Lačković, Milena and Petrović, Nina and Isenović, Esma R.",
year = "2018",
abstract = "Purpose: This study aimed to investigate in vivo effects of estradiol on the regulation of hepatic inducible nitric oxide synthase (iNOS) expression in the high fat (HF) diet-induced obesity. Also, we aimed to investigate whether activation of the extracellular signal-regulated kinase (ERK1/2), adenosine monophosphate-activated protein kinase (AMPK), Src kinase, and miR-221 is involved in estradiol-mediated regulation of iNOS in the liver of obese male Wistar rats. Male Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. Half of HF rats were treated with estradiol intraperitoneally (40 μg/kg), whereas the other half were placebo-treated 24 H before euthanasia. Results show that estradiol treatment of HF rats decreased hepatic iNOS mRNA (P < 0.05) and protein expression (P < 0.01), the protein levels of p65 subunit of nuclear factor κB (P < 0.05) and ERα (P < 0.05), ERK1/2 phosphorylation (P < 0.001), and ERα/Src kinase association (P < 0.05). By contrast, hepatic Src protein level (P < 0.05), AMPKα phosphorylation (P < 0.05), and miR-221 expression (P < 0.05) were increased in HF rats after estradiol treatment. Our results indicate that estradiol in vivo regulates hepatic iNOS expression in obese rats via molecular mechanisms involving ERK1/2, AMPK, Src, and miR-221 signaling. © 2018 International Union of Biochemistry and Molecular Biology, Inc.",
journal = "Biotechnology and Applied Biochemistry",
title = "Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221",
volume = "65",
number = "6",
pages = "797-806",
doi = "10.1002/bab.1680"
}

Panić, A., Stanimirović, J., Obradović, M. M., Sudar-Milovanović, E., Perović, M., Lačković, M., Petrović, N.,& Isenović, E. R.. (2018). Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221. in Biotechnology and Applied Biochemistry, 65(6), 797-806.
https://doi.org/10.1002/bab.1680

Panić A, Stanimirović J, Obradović MM, Sudar-Milovanović E, Perović M, Lačković M, Petrović N, Isenović ER. Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221. in Biotechnology and Applied Biochemistry. 2018;65(6):797-806.
doi:10.1002/bab.1680 .

Panić, Anastasija, Stanimirović, Julijana, Obradović, Milan M., Sudar-Milovanović, Emina, Perović, Milan, Lačković, Milena, Petrović, Nina, Isenović, Esma R., "Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221" in Biotechnology and Applied Biochemistry, 65, no. 6 (2018):797-806,
https://doi.org/10.1002/bab.1680 . .

TY  - CONF
AU  - Stanimirović, Julijana
AU  - Panić, Anastasija
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Isenović, Esma R.
PY  - 2018
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0021915018307147
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7948
C3  - Atherosclerosis
T1  - IGF-1 ameliorates detrimental effects of obesity in rat heart by promoting akt and FOXO1
VL  - 275
SP  - e137
DO  - 10.1016/j.atherosclerosis.2018.06.402
ER  - 

@conference{
author = "Stanimirović, Julijana and Panić, Anastasija and Obradović, Milan M. and Zafirović, Sonja and Isenović, Esma R.",
year = "2018",
journal = "Atherosclerosis",
title = "IGF-1 ameliorates detrimental effects of obesity in rat heart by promoting akt and FOXO1",
volume = "275",
pages = "e137",
doi = "10.1016/j.atherosclerosis.2018.06.402"
}

Stanimirović, J., Panić, A., Obradović, M. M., Zafirović, S.,& Isenović, E. R.. (2018). IGF-1 ameliorates detrimental effects of obesity in rat heart by promoting akt and FOXO1. in Atherosclerosis, 275, e137.
https://doi.org/10.1016/j.atherosclerosis.2018.06.402

Stanimirović J, Panić A, Obradović MM, Zafirović S, Isenović ER. IGF-1 ameliorates detrimental effects of obesity in rat heart by promoting akt and FOXO1. in Atherosclerosis. 2018;275:e137.
doi:10.1016/j.atherosclerosis.2018.06.402 .

Stanimirović, Julijana, Panić, Anastasija, Obradović, Milan M., Zafirović, Sonja, Isenović, Esma R., "IGF-1 ameliorates detrimental effects of obesity in rat heart by promoting akt and FOXO1" in Atherosclerosis, 275 (2018):e137,
https://doi.org/10.1016/j.atherosclerosis.2018.06.402 . .

TY  - JOUR
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7581
AB  - In this study, we assessed whether the disturbed regulation of sodium/potassium-adenosine-triphosphatase (Na+/K+-ATPase) occurs as a consequence of obesity-induced IR in sex-specific manner. We also assessed whether alterations of IRS/PI3K/Akt, ERK1/2, AMPK alpha, and RhoA/ROCK signaling cascades have an important role in this pathology. Female and male Wistar rats (150-200 g, 8 weeks old) were fed a standard laboratory diet or a high-fat (HF) diet (42% fat) for 10 weeks. The activity of hepatic Na+/K+-ATPase and Rho, and the association of IRS-1/p85 were assessed in liver. Furthermore, the protein level of alpha(1) Na+/K+-ATPase in plasma membrane fractions, and protein levels of IRS-1, PI3K-p85, -p110, RhoA, ROCK1, ROCK2, ERK1/2, AMPK alpha, ER alpha, and ER beta in liver lysates were assessed. The expression of hepatic alpha(1) Na+/K+-ATPase mRNA was also analyzed by qRT-PCR. The results show that HF-fed female rats exhibited an increase in hepatic ERK1/2 (p < 0.05) and AMPK alpha (p < 0.05) phosphorylation levels, unchanged level of Na+/K+-ATPase alpha(1) mRNA, decreased level of Na+/K+-ATPase activity (p < 0.05), and decreased alpha(1) Na+/K+-ATPase protein expression (p < 0.01). In liver of HF-fed male rats, results show decreased levels of Na+/K+-ATPase activity (p < 0.01), both protein and mRNA of alpha(1) subunit (p < 0.05), but significant increase in Rho activity (p < 0.05). Our results indicate significant sex differences in alpha(1) Na+/K+-ATPase mRNA expression and activation of ERK1/2, AMPK alpha, and Rho in the liver. Exploring the sex-specific factors and pathways that promote obesity-related diseases may lead to a better understanding of pathogenesis and discovering new therapeutic targets.
T2  - Molecular and Cellular Biochemistry
T1  - Regulation of hepatic Na+/K+-ATPase in obese female and male rats: involvement of ERK1/2, AMPK, and Rho/ROCK
VL  - 440
SP  - 77
EP  - 88
DO  - 10.1007/s11010-017-3157-z
ER  - 

@article{
year = "2018",
abstract = "In this study, we assessed whether the disturbed regulation of sodium/potassium-adenosine-triphosphatase (Na+/K+-ATPase) occurs as a consequence of obesity-induced IR in sex-specific manner. We also assessed whether alterations of IRS/PI3K/Akt, ERK1/2, AMPK alpha, and RhoA/ROCK signaling cascades have an important role in this pathology. Female and male Wistar rats (150-200 g, 8 weeks old) were fed a standard laboratory diet or a high-fat (HF) diet (42% fat) for 10 weeks. The activity of hepatic Na+/K+-ATPase and Rho, and the association of IRS-1/p85 were assessed in liver. Furthermore, the protein level of alpha(1) Na+/K+-ATPase in plasma membrane fractions, and protein levels of IRS-1, PI3K-p85, -p110, RhoA, ROCK1, ROCK2, ERK1/2, AMPK alpha, ER alpha, and ER beta in liver lysates were assessed. The expression of hepatic alpha(1) Na+/K+-ATPase mRNA was also analyzed by qRT-PCR. The results show that HF-fed female rats exhibited an increase in hepatic ERK1/2 (p < 0.05) and AMPK alpha (p < 0.05) phosphorylation levels, unchanged level of Na+/K+-ATPase alpha(1) mRNA, decreased level of Na+/K+-ATPase activity (p < 0.05), and decreased alpha(1) Na+/K+-ATPase protein expression (p < 0.01). In liver of HF-fed male rats, results show decreased levels of Na+/K+-ATPase activity (p < 0.01), both protein and mRNA of alpha(1) subunit (p < 0.05), but significant increase in Rho activity (p < 0.05). Our results indicate significant sex differences in alpha(1) Na+/K+-ATPase mRNA expression and activation of ERK1/2, AMPK alpha, and Rho in the liver. Exploring the sex-specific factors and pathways that promote obesity-related diseases may lead to a better understanding of pathogenesis and discovering new therapeutic targets.",
journal = "Molecular and Cellular Biochemistry",
title = "Regulation of hepatic Na+/K+-ATPase in obese female and male rats: involvement of ERK1/2, AMPK, and Rho/ROCK",
volume = "440",
pages = "77-88",
doi = "10.1007/s11010-017-3157-z"
}

(2018). Regulation of hepatic Na+/K+-ATPase in obese female and male rats: involvement of ERK1/2, AMPK, and Rho/ROCK. in Molecular and Cellular Biochemistry, 440, 77-88.
https://doi.org/10.1007/s11010-017-3157-z

Regulation of hepatic Na+/K+-ATPase in obese female and male rats: involvement of ERK1/2, AMPK, and Rho/ROCK. in Molecular and Cellular Biochemistry. 2018;440:77-88.
doi:10.1007/s11010-017-3157-z .

"Regulation of hepatic Na+/K+-ATPase in obese female and male rats: involvement of ERK1/2, AMPK, and Rho/ROCK" in Molecular and Cellular Biochemistry, 440 (2018):77-88,
https://doi.org/10.1007/s11010-017-3157-z . .

TY  - CONF
AU  - Panić, Anastasija
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Isenović, Esma R.
PY  - 2018
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0021915018307135
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7944
C3  - Atherosclerosis
T1  - IGF-1 regulates cardiac hypertrophy and inos expression in obese male rats through ERK1/2 signaling pathway
VL  - 275
SP  - e137
DO  - 10.1016/j.atherosclerosis.2018.06.401
ER  - 

@conference{
author = "Panić, Anastasija and Stanimirović, Julijana and Obradović, Milan M. and Sudar-Milovanović, Emina and Isenović, Esma R.",
year = "2018",
journal = "Atherosclerosis",
title = "IGF-1 regulates cardiac hypertrophy and inos expression in obese male rats through ERK1/2 signaling pathway",
volume = "275",
pages = "e137",
doi = "10.1016/j.atherosclerosis.2018.06.401"
}

Panić, A., Stanimirović, J., Obradović, M. M., Sudar-Milovanović, E.,& Isenović, E. R.. (2018). IGF-1 regulates cardiac hypertrophy and inos expression in obese male rats through ERK1/2 signaling pathway. in Atherosclerosis, 275, e137.
https://doi.org/10.1016/j.atherosclerosis.2018.06.401

Panić A, Stanimirović J, Obradović MM, Sudar-Milovanović E, Isenović ER. IGF-1 regulates cardiac hypertrophy and inos expression in obese male rats through ERK1/2 signaling pathway. in Atherosclerosis. 2018;275:e137.
doi:10.1016/j.atherosclerosis.2018.06.401 .

Panić, Anastasija, Stanimirović, Julijana, Obradović, Milan M., Sudar-Milovanović, Emina, Isenović, Esma R., "IGF-1 regulates cardiac hypertrophy and inos expression in obese male rats through ERK1/2 signaling pathway" in Atherosclerosis, 275 (2018):e137,
https://doi.org/10.1016/j.atherosclerosis.2018.06.401 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Stanimirović, Julijana
AU  - Panić, Anastasija
AU  - Bogdanović, Nikola
AU  - Sudar, Emina
AU  - Cenić-Milošević, Desanka
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1581
AB  - Background: The sodium/potassium- adenosine- triphosphatase (Na+/K+-ATPase) is an important mediator in vasculature tone and contractility, and its abnormal regulation has been implicated in many diseases such as obesity, insulin resistance, diabetes, and hypertension. Decreased Na+/K+-ATPase abundance and its altered isoform expression induce cardiomyocytes death and cardiac dysfunction, possibly leading to the development of myocardial dilation and heart failure. Therefore, the regulation of Na+/K+-ATPase activity/expression could be important in treatment and possible prevention of cardio-metabolic diseases. A number of hormones and environmental factors regulate the function of Na+/K+-ATPase in response to changing cellular requirements. Estradiol and insulin like growth factor-1 (IGF-1) are among potent hormones that positively regulate Na+/K+-ATPase activity or de novo synthesis of alpha -and beta -subunits. Both estradiol and IGF-1 have a huge therapeutic potential in treatment of vasculopathy in cardio-metabolic diseases. Methods: We searched the MEDLINE and PUBMED databases for all English and non-English articles with an English abstract from April 1978 to May 2016. The main data search terms were: Na+/K+-ATPase; estradiol and Na+/K+-ATPase; estradiol, Na+/K+-ATPase and CVS; estradiol, Na+/K+-ATPase and CVD; estradiol, Na+/K+-ATPase and obesity; estradiol, Na+/K+-ATPase and diabetes; estradiol, Na+/K+-ATPase and hypertension; IGF-1; IGF-1 and Na+/K+-ATPase; IGF-1, Na+/K+-ATPase and CVS; IGF-1, Na+/K+-ATPase and CVD; IGF-1, Na+/K+-ATPase and obesity; IGF-1, Na+/K+-ATPase and diabetes; IGF-1, Na+/K+-ATPase and hypertension. Results: The present review discusses the latest data from animal and human studies which focus on the effects of estradiol and IGF-1 on Na+/K+-ATPase regulation in physiological and pathophysiological conditions in cardiovascular system. Conclusion: Understanding the molecular mechanisms of estradiol and IGF-1 action on Na+/K+-ATPase in humans, may help resolving outstanding issues and developing new strategies for the protection and treatment of cardiovascular diseases.
T2  - Current Pharmaceutical Design
T1  - Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases
VL  - 23
IS  - 10
SP  - 1551
EP  - 1561
DO  - 10.2174/1381612823666170203113455
ER  - 

@article{
author = "Obradović, Milan M. and Stanimirović, Julijana and Panić, Anastasija and Bogdanović, Nikola and Sudar, Emina and Cenić-Milošević, Desanka and Isenović, Esma R.",
year = "2017",
abstract = "Background: The sodium/potassium- adenosine- triphosphatase (Na+/K+-ATPase) is an important mediator in vasculature tone and contractility, and its abnormal regulation has been implicated in many diseases such as obesity, insulin resistance, diabetes, and hypertension. Decreased Na+/K+-ATPase abundance and its altered isoform expression induce cardiomyocytes death and cardiac dysfunction, possibly leading to the development of myocardial dilation and heart failure. Therefore, the regulation of Na+/K+-ATPase activity/expression could be important in treatment and possible prevention of cardio-metabolic diseases. A number of hormones and environmental factors regulate the function of Na+/K+-ATPase in response to changing cellular requirements. Estradiol and insulin like growth factor-1 (IGF-1) are among potent hormones that positively regulate Na+/K+-ATPase activity or de novo synthesis of alpha -and beta -subunits. Both estradiol and IGF-1 have a huge therapeutic potential in treatment of vasculopathy in cardio-metabolic diseases. Methods: We searched the MEDLINE and PUBMED databases for all English and non-English articles with an English abstract from April 1978 to May 2016. The main data search terms were: Na+/K+-ATPase; estradiol and Na+/K+-ATPase; estradiol, Na+/K+-ATPase and CVS; estradiol, Na+/K+-ATPase and CVD; estradiol, Na+/K+-ATPase and obesity; estradiol, Na+/K+-ATPase and diabetes; estradiol, Na+/K+-ATPase and hypertension; IGF-1; IGF-1 and Na+/K+-ATPase; IGF-1, Na+/K+-ATPase and CVS; IGF-1, Na+/K+-ATPase and CVD; IGF-1, Na+/K+-ATPase and obesity; IGF-1, Na+/K+-ATPase and diabetes; IGF-1, Na+/K+-ATPase and hypertension. Results: The present review discusses the latest data from animal and human studies which focus on the effects of estradiol and IGF-1 on Na+/K+-ATPase regulation in physiological and pathophysiological conditions in cardiovascular system. Conclusion: Understanding the molecular mechanisms of estradiol and IGF-1 action on Na+/K+-ATPase in humans, may help resolving outstanding issues and developing new strategies for the protection and treatment of cardiovascular diseases.",
journal = "Current Pharmaceutical Design",
title = "Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases",
volume = "23",
number = "10",
pages = "1551-1561",
doi = "10.2174/1381612823666170203113455"
}

Obradović, M. M., Stanimirović, J., Panić, A., Bogdanović, N., Sudar, E., Cenić-Milošević, D.,& Isenović, E. R.. (2017). Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases. in Current Pharmaceutical Design, 23(10), 1551-1561.
https://doi.org/10.2174/1381612823666170203113455

Obradović MM, Stanimirović J, Panić A, Bogdanović N, Sudar E, Cenić-Milošević D, Isenović ER. Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases. in Current Pharmaceutical Design. 2017;23(10):1551-1561.
doi:10.2174/1381612823666170203113455 .

Obradović, Milan M., Stanimirović, Julijana, Panić, Anastasija, Bogdanović, Nikola, Sudar, Emina, Cenić-Milošević, Desanka, Isenović, Esma R., "Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases" in Current Pharmaceutical Design, 23, no. 10 (2017):1551-1561,
https://doi.org/10.2174/1381612823666170203113455 . .

TY  - JOUR
AU  - Sudar-Milovanović, Emina
AU  - Obradović, Milan M.
AU  - Jovanović, Aleksandra
AU  - Zarić, Božidarka
AU  - Zafirović, Sonja
AU  - Panić, Anastasija
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/829
AB  - The amino acid, L-Arginine (L-Arg) plays an important role in the cardiovascular system. Data from the literature show that L-Arg is the only substrate for the production of nitric oxide (NO), from which L-Arg develops its effects on the cardiovascular system. As a free radical, NO is synthesized in all mammalian cells by L-Arg with the activity of NO synthase (NOS). In states of hypertension, diabetes, hypercholesterolemia and vascular inflammation a disorder occurs in the metabolic pathway of the synthesis of NO from L-Arg which all together bring alterations of blood vessels. Experimental results obtained on animals, as well as clinical studies show that L-Arg has an effect on thrombocytes, on the process of coagulation and on the fibrolytic system. This mini review represents a summary of the latest scientific animal and human studies related to L-Arg and its mechanisms of actions with a focus on the role of L-Arg via NO pathway in cardiovascular disorders. Moreover, here we present data from recent animal and clinical studies suggesting that L-Arg could be one of the possible therapeutic molecules for improving the treatment of different cardiovascular disorders.
PB  - Bentham Science Publishers
T2  - Mini Reviews in Medicinal Chemistry
T1  - Benefits of L-Arginine on Cardiovascular System
VL  - 16
IS  - 2
SP  - 94
EP  - 103
DO  - 10.2174/1389557515666151016125826
ER  - 

@article{
author = "Sudar-Milovanović, Emina and Obradović, Milan M. and Jovanović, Aleksandra and Zarić, Božidarka and Zafirović, Sonja and Panić, Anastasija and Radak, Đorđe J. and Isenović, Esma R.",
year = "2016",
abstract = "The amino acid, L-Arginine (L-Arg) plays an important role in the cardiovascular system. Data from the literature show that L-Arg is the only substrate for the production of nitric oxide (NO), from which L-Arg develops its effects on the cardiovascular system. As a free radical, NO is synthesized in all mammalian cells by L-Arg with the activity of NO synthase (NOS). In states of hypertension, diabetes, hypercholesterolemia and vascular inflammation a disorder occurs in the metabolic pathway of the synthesis of NO from L-Arg which all together bring alterations of blood vessels. Experimental results obtained on animals, as well as clinical studies show that L-Arg has an effect on thrombocytes, on the process of coagulation and on the fibrolytic system. This mini review represents a summary of the latest scientific animal and human studies related to L-Arg and its mechanisms of actions with a focus on the role of L-Arg via NO pathway in cardiovascular disorders. Moreover, here we present data from recent animal and clinical studies suggesting that L-Arg could be one of the possible therapeutic molecules for improving the treatment of different cardiovascular disorders.",
publisher = "Bentham Science Publishers",
journal = "Mini Reviews in Medicinal Chemistry",
title = "Benefits of L-Arginine on Cardiovascular System",
volume = "16",
number = "2",
pages = "94-103",
doi = "10.2174/1389557515666151016125826"
}

Sudar-Milovanović, E., Obradović, M. M., Jovanović, A., Zarić, B., Zafirović, S., Panić, A., Radak, Đ. J.,& Isenović, E. R.. (2016). Benefits of L-Arginine on Cardiovascular System. in Mini Reviews in Medicinal Chemistry
Bentham Science Publishers., 16(2), 94-103.
https://doi.org/10.2174/1389557515666151016125826

Sudar-Milovanović E, Obradović MM, Jovanović A, Zarić B, Zafirović S, Panić A, Radak ĐJ, Isenović ER. Benefits of L-Arginine on Cardiovascular System. in Mini Reviews in Medicinal Chemistry. 2016;16(2):94-103.
doi:10.2174/1389557515666151016125826 .

Sudar-Milovanović, Emina, Obradović, Milan M., Jovanović, Aleksandra, Zarić, Božidarka, Zafirović, Sonja, Panić, Anastasija, Radak, Đorđe J., Isenović, Esma R., "Benefits of L-Arginine on Cardiovascular System" in Mini Reviews in Medicinal Chemistry, 16, no. 2 (2016):94-103,
https://doi.org/10.2174/1389557515666151016125826 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Gluvić, Zoran
AU  - Sudar, Emina
AU  - Panić, Anastasija
AU  - Trebaljevac, Jovana
AU  - Bajić, Vladan P.
AU  - Zarkovic, Milos
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1006
AB  - Subclinical hypothyroidism (SH) is characterized by a mildly elevated concentration of thyroid stimulating hormone (TSH) despite free thyroxine (FT4) and triiodothyronine (FT3) levels within the reference range. Numerous studies revealed SH to be an independent risk factor for cardiovascular disease (CVD),including atherosclerosis, congestive heart failure, coronary heart disease, ischemic heart disease and the associated mortality. The relationship between SH and CVD is well documented, but the molecular mechanism underlying this correlation remain unknown. Endothelial dysfunction has been recognized as an initial step leading to CVD in patients with SH. Changes in lipid profile, inflammation and/or oxidative stress contribute to the endothelial dysfunction in SH. Moreover, the progression of SH is characterized by significantly decreased nitrite and nitrate levels. Recent animal and clinical studies discussed in this review suggest that nitric oxide (NO) levels could be a reliable biomarker for cardiovascular risk in SH. Understanding the regulation of NO production by thyroid hormone may provide novel and useful knowledge regarding how endothelial dysfunction in SH is linked with CVD and help us to uncover new treatments for SH. We suggest that serum NO level may be an indicator for the introduction and dosage of levothyroxine (LT4) replacement therapy in SH patients. Future studies should focus on understanding the molecular mechanisms underlying the effects of NO in physiological as well as in pathophysiological conditions such as hypothyroidism and their clinical relevance.
T2  - Current Vascular Pharmacology
T1  - Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients
VL  - 14
IS  - 3
SP  - 266
EP  - 270
DO  - 10.2174/1570161114666160208143537
ER  - 

@article{
author = "Obradović, Milan M. and Gluvić, Zoran and Sudar, Emina and Panić, Anastasija and Trebaljevac, Jovana and Bajić, Vladan P. and Zarkovic, Milos and Isenović, Esma R.",
year = "2016",
abstract = "Subclinical hypothyroidism (SH) is characterized by a mildly elevated concentration of thyroid stimulating hormone (TSH) despite free thyroxine (FT4) and triiodothyronine (FT3) levels within the reference range. Numerous studies revealed SH to be an independent risk factor for cardiovascular disease (CVD),including atherosclerosis, congestive heart failure, coronary heart disease, ischemic heart disease and the associated mortality. The relationship between SH and CVD is well documented, but the molecular mechanism underlying this correlation remain unknown. Endothelial dysfunction has been recognized as an initial step leading to CVD in patients with SH. Changes in lipid profile, inflammation and/or oxidative stress contribute to the endothelial dysfunction in SH. Moreover, the progression of SH is characterized by significantly decreased nitrite and nitrate levels. Recent animal and clinical studies discussed in this review suggest that nitric oxide (NO) levels could be a reliable biomarker for cardiovascular risk in SH. Understanding the regulation of NO production by thyroid hormone may provide novel and useful knowledge regarding how endothelial dysfunction in SH is linked with CVD and help us to uncover new treatments for SH. We suggest that serum NO level may be an indicator for the introduction and dosage of levothyroxine (LT4) replacement therapy in SH patients. Future studies should focus on understanding the molecular mechanisms underlying the effects of NO in physiological as well as in pathophysiological conditions such as hypothyroidism and their clinical relevance.",
journal = "Current Vascular Pharmacology",
title = "Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients",
volume = "14",
number = "3",
pages = "266-270",
doi = "10.2174/1570161114666160208143537"
}

Obradović, M. M., Gluvić, Z., Sudar, E., Panić, A., Trebaljevac, J., Bajić, V. P., Zarkovic, M.,& Isenović, E. R.. (2016). Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients. in Current Vascular Pharmacology, 14(3), 266-270.
https://doi.org/10.2174/1570161114666160208143537

Obradović MM, Gluvić Z, Sudar E, Panić A, Trebaljevac J, Bajić VP, Zarkovic M, Isenović ER. Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients. in Current Vascular Pharmacology. 2016;14(3):266-270.
doi:10.2174/1570161114666160208143537 .

Obradović, Milan M., Gluvić, Zoran, Sudar, Emina, Panić, Anastasija, Trebaljevac, Jovana, Bajić, Vladan P., Zarkovic, Milos, Isenović, Esma R., "Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients" in Current Vascular Pharmacology, 14, no. 3 (2016):266-270,
https://doi.org/10.2174/1570161114666160208143537 . .

TY  - JOUR
AU  - Resanović, Ivana
AU  - Sudar-Milovanović, Emina
AU  - Bogdanović, Nikola
AU  - Jovanović, Aleksandra
AU  - Zafirović, Sonja
AU  - Panić, Anastasija
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10316
AB  - Apoptoza je evolutivno očuvan mehanizam programirane ćelijske smrti, koji ima važnu ulogu u fiziološkim procesima, kao što su embrionalno razviće, hromonima regulisana ćelijska smrt, funkcionisanje imunog sistema i uklanjanje oštećenih ćelija. Dva osnovna puta indukcije apoptoze su unutrašnji i spoljašnji. Dok unutrašnji put apoptoze može pokrenuti unutarćeljska akumulacija Ca 2+ jona, koja je praćena permeabilizacijom membrane mitohondrija i oslobađanjem pro-apoptotskih proteina iz mitohondrija u citoplazmu, spoljašnji put uključuje aktivaciju membransih receptora za TNF-a (engl. Tumor Necrosis Factor-a), kao što su TNFR-1 (engl. Tumor Necrosis Factor receptor 1), Fas, i TRAIL-R (engl. TNF-related apoptosis-inducing ligand receptors). Pored toga, postoji i perforin-granzim put koji uključuje aktivaciju citotoksičnih T-limfocita. Sva tri puta rezultiraju fragmentacijom DNK, degradacijom citoskeleta i nuklearnih proteina, unakrsnim povezivanjem proteina, formiranjem apoptotskih tela, ekspresijom liganada za receptore na fagocitima i na kraju fagocitozom. U ovoj reviji su objedinjeni podaci iz nedavno objavljenih studija koje su fokusirane na proteine uključene u proces apoptoze i molekularne mehanizme apoptoze. Razumevanje mehanizama apoptoze može da pruži korisne informacije i nove pristupe u prevenciji i razvoju novih terapija za različite bolesti.
AB  - Apoptosis is evolutionary conserved, programmed pattern of cell death with an essential role in various physiological processes, such as normal cell turnover and embryonic development, hormone-regulated cell demise, aging, immune system functioning and development and removal of defective and harmful cells. There are two general pathways for activation of apoptosis: the intrinsic and extrinsic pathways. While the intrinsic apoptotic pathway can be triggered by a cytotoxic accumulation of intracellular Ca 2+ , followed permeabilization of mitochondrial membrane and release of pro-apoptotic proteins into the cytosol from mitochondria, the extrinsic mechanisms of apoptosis include the participation of death receptors of tumor necrosis factor-a (TNF-a), receptor superfamily such as TNFR-1, Fas, and TNF-related apoptosis-inducing ligand receptors (TRAIL-R) located on the plasma membrane. There is also the perforin-granzyme pathway that involves T-cell mediated cytotoxicity. All three pathways converge on the same execution pathway, resulting in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. In this review we summarize data from recent studies focusing on apoptotic proteins that have been identified and molecular mechanisms of apoptosis. Understanding apoptotic mechanism might provide useful information and a new approach to prevention and development of new therapies for variety of diseases.
T2  - Medicinska istraživanja
T1  - Osnove apoptoze
T1  - Fundamentals of apoptosis
VL  - 49
IS  - 2
SP  - 42
EP  - 45
DO  - 10.5937/MedIst1502042R
ER  - 

@article{
author = "Resanović, Ivana and Sudar-Milovanović, Emina and Bogdanović, Nikola and Jovanović, Aleksandra and Zafirović, Sonja and Panić, Anastasija and Isenović, Esma R.",
year = "2015",
abstract = "Apoptoza je evolutivno očuvan mehanizam programirane ćelijske smrti, koji ima važnu ulogu u fiziološkim procesima, kao što su embrionalno razviće, hromonima regulisana ćelijska smrt, funkcionisanje imunog sistema i uklanjanje oštećenih ćelija. Dva osnovna puta indukcije apoptoze su unutrašnji i spoljašnji. Dok unutrašnji put apoptoze može pokrenuti unutarćeljska akumulacija Ca 2+ jona, koja je praćena permeabilizacijom membrane mitohondrija i oslobađanjem pro-apoptotskih proteina iz mitohondrija u citoplazmu, spoljašnji put uključuje aktivaciju membransih receptora za TNF-a (engl. Tumor Necrosis Factor-a), kao što su TNFR-1 (engl. Tumor Necrosis Factor receptor 1), Fas, i TRAIL-R (engl. TNF-related apoptosis-inducing ligand receptors). Pored toga, postoji i perforin-granzim put koji uključuje aktivaciju citotoksičnih T-limfocita. Sva tri puta rezultiraju fragmentacijom DNK, degradacijom citoskeleta i nuklearnih proteina, unakrsnim povezivanjem proteina, formiranjem apoptotskih tela, ekspresijom liganada za receptore na fagocitima i na kraju fagocitozom. U ovoj reviji su objedinjeni podaci iz nedavno objavljenih studija koje su fokusirane na proteine uključene u proces apoptoze i molekularne mehanizme apoptoze. Razumevanje mehanizama apoptoze može da pruži korisne informacije i nove pristupe u prevenciji i razvoju novih terapija za različite bolesti., Apoptosis is evolutionary conserved, programmed pattern of cell death with an essential role in various physiological processes, such as normal cell turnover and embryonic development, hormone-regulated cell demise, aging, immune system functioning and development and removal of defective and harmful cells. There are two general pathways for activation of apoptosis: the intrinsic and extrinsic pathways. While the intrinsic apoptotic pathway can be triggered by a cytotoxic accumulation of intracellular Ca 2+ , followed permeabilization of mitochondrial membrane and release of pro-apoptotic proteins into the cytosol from mitochondria, the extrinsic mechanisms of apoptosis include the participation of death receptors of tumor necrosis factor-a (TNF-a), receptor superfamily such as TNFR-1, Fas, and TNF-related apoptosis-inducing ligand receptors (TRAIL-R) located on the plasma membrane. There is also the perforin-granzyme pathway that involves T-cell mediated cytotoxicity. All three pathways converge on the same execution pathway, resulting in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. In this review we summarize data from recent studies focusing on apoptotic proteins that have been identified and molecular mechanisms of apoptosis. Understanding apoptotic mechanism might provide useful information and a new approach to prevention and development of new therapies for variety of diseases.",
journal = "Medicinska istraživanja",
title = "Osnove apoptoze, Fundamentals of apoptosis",
volume = "49",
number = "2",
pages = "42-45",
doi = "10.5937/MedIst1502042R"
}

Resanović, I., Sudar-Milovanović, E., Bogdanović, N., Jovanović, A., Zafirović, S., Panić, A.,& Isenović, E. R.. (2015). Osnove apoptoze. in Medicinska istraživanja, 49(2), 42-45.
https://doi.org/10.5937/MedIst1502042R

Resanović I, Sudar-Milovanović E, Bogdanović N, Jovanović A, Zafirović S, Panić A, Isenović ER. Osnove apoptoze. in Medicinska istraživanja. 2015;49(2):42-45.
doi:10.5937/MedIst1502042R .

Resanović, Ivana, Sudar-Milovanović, Emina, Bogdanović, Nikola, Jovanović, Aleksandra, Zafirović, Sonja, Panić, Anastasija, Isenović, Esma R., "Osnove apoptoze" in Medicinska istraživanja, 49, no. 2 (2015):42-45,
https://doi.org/10.5937/MedIst1502042R . .

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  - Popin-Tarić, Marija
AU  - Gluvić, Zoran
AU  - Samardžić, Vladimir
AU  - Vasić-Vlaisavljević, Anita
AU  - Tica-Jevtić, Jelena
AU  - Panić, Anastasija
AU  - Sudar-Milovanović, Emina
AU  - Tomašević, Ratko
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10313
AB  - Uvod: Poznat je uticaj manifestnih tireoidnih disfunkcija na promene u koštanoj masi koji se ispoljava kroz izmene u koštanom prometu, koje dovode do promena koštane gustine i mogućeg povećanog rizika od pada i preloma. Takođe, uticajem na metaboličke parametre, prevashodno na lipide, tireoidne disfunkcije predstavljaju važan uzrok akceleracije ateroskleroze i povećanja cerebrovaskularnog i kardiovaskularnog rizika. Ovom studijom je ispitivan metabolički profil i koštana gustina kod pacijenata sa dijagnostikovanom supkliničkom tireoidnom disfunkcijom. Materijal i metode: Pilot studija preseka obuhvatila je 45 selektovanih ispitanica, koje su ispunile inkluzione kriterijume. Na osnovu nivoa tireo-stimulišućeg hormona (TSH) i slobodnog tiroksina (fT4) ispitanice su svrstane u 3 grupe, po 15 ispitanica u svakoj grupi: -grupa: supklinička hipotireoza (SHipo), grupa: supklinička hipertireoza (SHiper), i grupa: eutireodna-tj. kontrolna grupa. Od faktora rizika, praćeni su godine života, podaci o menopauzi i prethodnim prelomima, a od metaboličkih parametara indeks telesne mase (engl. Body Mass Index, BMI), obim struka (OS), obim kuka (OK), nivo tri-glicerida i nivo ukupnog holesterola. Kod svih ispitanica je merena koštana gustina na lumbalnoj kičmi i levom kuku (LK) i izražena u T skorovima. Dobijeni podaci su analizirani koriščćenjem statističkog paketa SPSS za Windows. Statistički značajnom je smatrana verovatnoća manja od 0,05 (p<0,05). Rezultati: Grupe ispitanica su se značajno razlikovale po nivoima ukupnog holesterola, kao i T skorovima lumbalne kičme i LK. Smanjena koštana gustina je registrovana kod 35 (77,8%) ispitanica. Vrednosti T skorova lumbalne kičme i LK su unutargrupno međusobno korelisali. Od faktora rizika, postojanje prethodnih preloma i menopauze, značajno utiču na T skorove, što nije slučaj ni sa jednim metaboličkim parametrom. Najniži T skorovi, kao i sa kliničkog aspekta najznačajnija dislipidemija, su registrovani u grupi SHipo. Diskusija: U okviru ove pilot studije pokazano je smanjenje koštane gustine u populaciji ispitanica sa supkliničkim tireoidopatijama, najviše izražena u SHipo grupi. U istoj grupi je zabeležen i klinički najaterogeniji lipidni profil (hiperholesterolemija). Metabolički parametri kao i hormoni nisu uticali na T skorove lumbalne kičme i LK. Zaključak: Supkliničke tireoidne disfunkcije su povezane sa smanjenjem koštane gustine, izražene kroz T skorove na lumbalnoj kičmi i LK, i na njih nisu uticali metabolički parametri. Pravovremenom dijagnostikom i lečenjem tireoidnih disfunkcija, moguće je usporiti gubitak koštane mase, smanjiti rizik kako od pada tako i od preloma, pri čemu korekcijom lipidnog disbalansa se može smanjiti potencijalni cerebrovaskularni i kardiovaskularni rizik.
AB  - Introduction. It is well-known that overt thyroid dysfunctions have an influence on bone mineral density (BMD). It is noticed as a change in bone turnover and BMD, with subsequent increased risk of fall-induced fractures. Additionally, promoting the lipid profile derangement, subclinical thyroid dysfunction seems to be an important factor of atherosclerosis acceleration and the risk of cerebrovascular and cardiovascular incidents. In this study we examined the relationship between some of osteoporosis risk factors, metabolic parameters and BMD, in subclinical thyroidopathies. Material and Methods. Pilot cross-sectional study involved 45 females selected on fulfilled inclusion criteria. Three groups of 15 examinees were formed, based on TSH and fT4 serum levels (SHypo, SHyper, and euthyroid-control). As for risk factors, age, records on menopause and history of past fractures as well as metabolic parameters Body Mass Index (BMI), waist and hip circumference, cholesterol and triglyceride levels were observed. The entire study population was referred to DEXA (Dual Energy X Ray Absorptiometry) scan for BMD measurement on lumbar spine (LS) and left hip (LH), expressed through T scores. The obtained data were analyzed by SPSS for Windows 18.0 statistical package. The level of statistical significance was 0.05. Results. The groups of patients differed on cholesterol levels and LS/LH T scores. Decreased BMD was detected in 35 (77.4%) patients. Intergroup correlations of LS/LH T scores were registered. A history of past fractures and records on menopause significantly influenced LS/LH T scores, which was not the case with metabolic parameters. Both the lowest T scores and clinically important dyslipidemia were presented in SHypo group. Discussion. The pilot study pointed out a decrease in BMD (mostly on osteopenia level) in subclinical, presumably hypothyroid disorder. The presence of hypercholesterolemia was detected in the same group. Metabolic parameters and thyroid hormones (TSH and fT4) did not have an effect on BMD. Conclusion. Subclinical thyroid dysfunctions are associated with a decrease in BMD, mostly presented as osteopenia, with a higher degree of severity in SHypo group. There is no registered influence of metabolic parameters on LS/LH T scores. It can be possible to slow down progression of decrease in BMD and subsequent fracture risk, with proper diagnostics and management of subclinical thyroid dysfunctions. Additionally, with correction of lipid disorders, cardiovascular and cerebrovascular risk could be minimized.
T2  - Medicinska istraživanja
T1  - Korelacija metaboličkog profila i koštane gustine kod netretiranih ispitanica obolelih od supkliničkih tireoidnih disfunkcija - pilot studija
T1  - Correlation of metabolic profile and Bone mineral density in treatment: Naive females with subclinical thyroid dysfunction: A pilot study
VL  - 49
IS  - 2
SP  - 50
EP  - 57
DO  - 10.5937/MedIst1502050P
ER  - 

@article{
author = "Popin-Tarić, Marija and Gluvić, Zoran and Samardžić, Vladimir and Vasić-Vlaisavljević, Anita and Tica-Jevtić, Jelena and Panić, Anastasija and Sudar-Milovanović, Emina and Tomašević, Ratko and Isenović, Esma R.",
year = "2015",
abstract = "Uvod: Poznat je uticaj manifestnih tireoidnih disfunkcija na promene u koštanoj masi koji se ispoljava kroz izmene u koštanom prometu, koje dovode do promena koštane gustine i mogućeg povećanog rizika od pada i preloma. Takođe, uticajem na metaboličke parametre, prevashodno na lipide, tireoidne disfunkcije predstavljaju važan uzrok akceleracije ateroskleroze i povećanja cerebrovaskularnog i kardiovaskularnog rizika. Ovom studijom je ispitivan metabolički profil i koštana gustina kod pacijenata sa dijagnostikovanom supkliničkom tireoidnom disfunkcijom. Materijal i metode: Pilot studija preseka obuhvatila je 45 selektovanih ispitanica, koje su ispunile inkluzione kriterijume. Na osnovu nivoa tireo-stimulišućeg hormona (TSH) i slobodnog tiroksina (fT4) ispitanice su svrstane u 3 grupe, po 15 ispitanica u svakoj grupi: -grupa: supklinička hipotireoza (SHipo), grupa: supklinička hipertireoza (SHiper), i grupa: eutireodna-tj. kontrolna grupa. Od faktora rizika, praćeni su godine života, podaci o menopauzi i prethodnim prelomima, a od metaboličkih parametara indeks telesne mase (engl. Body Mass Index, BMI), obim struka (OS), obim kuka (OK), nivo tri-glicerida i nivo ukupnog holesterola. Kod svih ispitanica je merena koštana gustina na lumbalnoj kičmi i levom kuku (LK) i izražena u T skorovima. Dobijeni podaci su analizirani koriščćenjem statističkog paketa SPSS za Windows. Statistički značajnom je smatrana verovatnoća manja od 0,05 (p<0,05). Rezultati: Grupe ispitanica su se značajno razlikovale po nivoima ukupnog holesterola, kao i T skorovima lumbalne kičme i LK. Smanjena koštana gustina je registrovana kod 35 (77,8%) ispitanica. Vrednosti T skorova lumbalne kičme i LK su unutargrupno međusobno korelisali. Od faktora rizika, postojanje prethodnih preloma i menopauze, značajno utiču na T skorove, što nije slučaj ni sa jednim metaboličkim parametrom. Najniži T skorovi, kao i sa kliničkog aspekta najznačajnija dislipidemija, su registrovani u grupi SHipo. Diskusija: U okviru ove pilot studije pokazano je smanjenje koštane gustine u populaciji ispitanica sa supkliničkim tireoidopatijama, najviše izražena u SHipo grupi. U istoj grupi je zabeležen i klinički najaterogeniji lipidni profil (hiperholesterolemija). Metabolički parametri kao i hormoni nisu uticali na T skorove lumbalne kičme i LK. Zaključak: Supkliničke tireoidne disfunkcije su povezane sa smanjenjem koštane gustine, izražene kroz T skorove na lumbalnoj kičmi i LK, i na njih nisu uticali metabolički parametri. Pravovremenom dijagnostikom i lečenjem tireoidnih disfunkcija, moguće je usporiti gubitak koštane mase, smanjiti rizik kako od pada tako i od preloma, pri čemu korekcijom lipidnog disbalansa se može smanjiti potencijalni cerebrovaskularni i kardiovaskularni rizik., Introduction. It is well-known that overt thyroid dysfunctions have an influence on bone mineral density (BMD). It is noticed as a change in bone turnover and BMD, with subsequent increased risk of fall-induced fractures. Additionally, promoting the lipid profile derangement, subclinical thyroid dysfunction seems to be an important factor of atherosclerosis acceleration and the risk of cerebrovascular and cardiovascular incidents. In this study we examined the relationship between some of osteoporosis risk factors, metabolic parameters and BMD, in subclinical thyroidopathies. Material and Methods. Pilot cross-sectional study involved 45 females selected on fulfilled inclusion criteria. Three groups of 15 examinees were formed, based on TSH and fT4 serum levels (SHypo, SHyper, and euthyroid-control). As for risk factors, age, records on menopause and history of past fractures as well as metabolic parameters Body Mass Index (BMI), waist and hip circumference, cholesterol and triglyceride levels were observed. The entire study population was referred to DEXA (Dual Energy X Ray Absorptiometry) scan for BMD measurement on lumbar spine (LS) and left hip (LH), expressed through T scores. The obtained data were analyzed by SPSS for Windows 18.0 statistical package. The level of statistical significance was 0.05. Results. The groups of patients differed on cholesterol levels and LS/LH T scores. Decreased BMD was detected in 35 (77.4%) patients. Intergroup correlations of LS/LH T scores were registered. A history of past fractures and records on menopause significantly influenced LS/LH T scores, which was not the case with metabolic parameters. Both the lowest T scores and clinically important dyslipidemia were presented in SHypo group. Discussion. The pilot study pointed out a decrease in BMD (mostly on osteopenia level) in subclinical, presumably hypothyroid disorder. The presence of hypercholesterolemia was detected in the same group. Metabolic parameters and thyroid hormones (TSH and fT4) did not have an effect on BMD. Conclusion. Subclinical thyroid dysfunctions are associated with a decrease in BMD, mostly presented as osteopenia, with a higher degree of severity in SHypo group. There is no registered influence of metabolic parameters on LS/LH T scores. It can be possible to slow down progression of decrease in BMD and subsequent fracture risk, with proper diagnostics and management of subclinical thyroid dysfunctions. Additionally, with correction of lipid disorders, cardiovascular and cerebrovascular risk could be minimized.",
journal = "Medicinska istraživanja",
title = "Korelacija metaboličkog profila i koštane gustine kod netretiranih ispitanica obolelih od supkliničkih tireoidnih disfunkcija - pilot studija, Correlation of metabolic profile and Bone mineral density in treatment: Naive females with subclinical thyroid dysfunction: A pilot study",
volume = "49",
number = "2",
pages = "50-57",
doi = "10.5937/MedIst1502050P"
}

Popin-Tarić, M., Gluvić, Z., Samardžić, V., Vasić-Vlaisavljević, A., Tica-Jevtić, J., Panić, A., Sudar-Milovanović, E., Tomašević, R.,& Isenović, E. R.. (2015). Korelacija metaboličkog profila i koštane gustine kod netretiranih ispitanica obolelih od supkliničkih tireoidnih disfunkcija - pilot studija. in Medicinska istraživanja, 49(2), 50-57.
https://doi.org/10.5937/MedIst1502050P

Popin-Tarić M, Gluvić Z, Samardžić V, Vasić-Vlaisavljević A, Tica-Jevtić J, Panić A, Sudar-Milovanović E, Tomašević R, Isenović ER. Korelacija metaboličkog profila i koštane gustine kod netretiranih ispitanica obolelih od supkliničkih tireoidnih disfunkcija - pilot studija. in Medicinska istraživanja. 2015;49(2):50-57.
doi:10.5937/MedIst1502050P .

Popin-Tarić, Marija, Gluvić, Zoran, Samardžić, Vladimir, Vasić-Vlaisavljević, Anita, Tica-Jevtić, Jelena, Panić, Anastasija, Sudar-Milovanović, Emina, Tomašević, Ratko, Isenović, Esma R., "Korelacija metaboličkog profila i koštane gustine kod netretiranih ispitanica obolelih od supkliničkih tireoidnih disfunkcija - pilot studija" in Medicinska istraživanja, 49, no. 2 (2015):50-57,
https://doi.org/10.5937/MedIst1502050P . .

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 . .