TY  - JOUR
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Jovanović, Aleksandra
AU  - Trebaljevac, Jovana
AU  - Obradović, Milan M.
AU  - Cenić-Milošević, Desanka
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1580
AB  - Background: Nitric oxide (NO) is a potential biochemical, cardio-metabolic risk marker. The production of NO is catalyzed by different isoforms of enzymes, NO synthases (NOS). An altered NO level is associated with obesity, insulin resistance (IR), diabetes and cardiovascular diseases (CVD). Activity of NOS and NO production are regulated by various hormones under physiological and pathophysiological condition. Methods: Data used for this review were obtained by searching the electronic database [PUBMED/MEDLINE 1984 - May 2016]. Additionally, abstracts from national and international diabetes and cardiovascular related meetings were searched. The main data search terms were: nitric oxide, nitric oxide synthase, cardio-metabolic risk, obesity, diabetes, cardiovascular disease, estradiol and insulin-like growth factor-1. Results: In this review, we summarize the recent literature data related to the regulation of endothelial NOS (eNOS), inducible (iNOS) activity/expression, and thereby NO production by the hormones: estradiol (E2), and insulin-like growth factor-1 (IGF-1). Conclusion: Understanding the regulation of NO production by different hormones such as E2, and IGF-1 may provide novel and useful knowledge regarding how endothelial dysfunction (ED) is linked with cardio-metabolic alterations and diseases.
T2  - Current Pharmaceutical Design
T1  - Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases
VL  - 23
IS  - 10
SP  - 1427
EP  - 1434
DO  - 10.2174/1381612823666170124124855
ER  - 

@article{
author = "Sudar, Emina and Zafirović, Sonja and Jovanović, Aleksandra and Trebaljevac, Jovana and Obradović, Milan M. and Cenić-Milošević, Desanka and Isenović, Esma R.",
year = "2017",
abstract = "Background: Nitric oxide (NO) is a potential biochemical, cardio-metabolic risk marker. The production of NO is catalyzed by different isoforms of enzymes, NO synthases (NOS). An altered NO level is associated with obesity, insulin resistance (IR), diabetes and cardiovascular diseases (CVD). Activity of NOS and NO production are regulated by various hormones under physiological and pathophysiological condition. Methods: Data used for this review were obtained by searching the electronic database [PUBMED/MEDLINE 1984 - May 2016]. Additionally, abstracts from national and international diabetes and cardiovascular related meetings were searched. The main data search terms were: nitric oxide, nitric oxide synthase, cardio-metabolic risk, obesity, diabetes, cardiovascular disease, estradiol and insulin-like growth factor-1. Results: In this review, we summarize the recent literature data related to the regulation of endothelial NOS (eNOS), inducible (iNOS) activity/expression, and thereby NO production by the hormones: estradiol (E2), and insulin-like growth factor-1 (IGF-1). Conclusion: Understanding the regulation of NO production by different hormones such as E2, and IGF-1 may provide novel and useful knowledge regarding how endothelial dysfunction (ED) is linked with cardio-metabolic alterations and diseases.",
journal = "Current Pharmaceutical Design",
title = "Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases",
volume = "23",
number = "10",
pages = "1427-1434",
doi = "10.2174/1381612823666170124124855"
}

Sudar, E., Zafirović, S., Jovanović, A., Trebaljevac, J., Obradović, M. M., Cenić-Milošević, D.,& Isenović, E. R.. (2017). Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases. in Current Pharmaceutical Design, 23(10), 1427-1434.
https://doi.org/10.2174/1381612823666170124124855

Sudar E, Zafirović S, Jovanović A, Trebaljevac J, Obradović MM, Cenić-Milošević D, Isenović ER. Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases. in Current Pharmaceutical Design. 2017;23(10):1427-1434.
doi:10.2174/1381612823666170124124855 .

Sudar, Emina, Zafirović, Sonja, Jovanović, Aleksandra, Trebaljevac, Jovana, Obradović, Milan M., Cenić-Milošević, Desanka, Isenović, Esma R., "Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases" in Current Pharmaceutical Design, 23, no. 10 (2017):1427-1434,
https://doi.org/10.2174/1381612823666170124124855 . .

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  - Gluvić, Zoran
AU  - Kovačević, Pejka
AU  - Obradović, Milan M.
AU  - Trebaljevac, Jovana
AU  - Samardžić, Vladimir
AU  - Lačković, Milena
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10152
AB  - Akutni infarkt miokarda (AIM) je klinički oblik koronarne bolesti srca, koji nastaje pri okluziji koronarne arterije, a ireverzibilna ishemija progredira do nekroze miokarda. Morbiditet i mortalitet od kardiovaskularnih komorbiditeta, uključujući AIM, je kod obolelih od insulin-nezavisnog dijabetesa veći nego kod nedijabetičara iste životne dobi. Jedan od razloga za veći mortalitet od infarkta miokarda kod dijabetičara može biti i srčana insuficijencija. Bolesnici sa diajbetesom i AIM imaju povećan rizik od lošeg ishoda terapije AIM u odnosu na nedijabetičare, a osnovni razlozi su endotelna disfunkcija, protrombotično stanje, veća mogućnost restenoze, negativnog vaskularnog remodelovanja, povećane glikolizacije proteinai depozicije vaskularnog matriksa. U okviru ovog preglednog članka, dat je prikaz najnovijih literaturnih podataka i praktičnih saznanja o AIM kod dijabetičnih bolesnika.
AB  - Acute myocardial infarction (AMI) is a clinical form of coronary heart disease, which occurs after coronary arteries' occlusion and irreversible ischemia progression leads to myocardial necrosis. Morbidity and mortality caused by cardiovascular comorbidities, including AIM, are greater in patients with insulin - dependent diabetes than in non - diabetes patients of the same age. One of the reasons for a higher mortality rate from AMI in patients with diabetes may be heart failure. In addition, patients with diabetes and AMI have an increased risk for poor therapy outcomes of AMI compared with non - diabetes patients, and the main reasons are endothelial dysfunction, prothrombotic state, a greater possibility of restenosis, negative vascular remodelling, increased protein glycosylation, and vascular matrix deposition. In this review, we provide an overview of recent literature data and practical knowledge related to the AMI in diabetic patients.
T2  - Medicinska istraživanja
T1  - Akutni infarkt miokarda i diabetes mellitus
T1  - Acute myocardial infarction and diabetes mellitus
VL  - 49
IS  - 3
SP  - 16
EP  - 19
DO  - 10.5937/MedIst1503016G
ER  - 

@article{
author = "Gluvić, Zoran and Kovačević, Pejka and Obradović, Milan M. and Trebaljevac, Jovana and Samardžić, Vladimir and Lačković, Milena and Isenović, Esma R.",
year = "2015",
abstract = "Akutni infarkt miokarda (AIM) je klinički oblik koronarne bolesti srca, koji nastaje pri okluziji koronarne arterije, a ireverzibilna ishemija progredira do nekroze miokarda. Morbiditet i mortalitet od kardiovaskularnih komorbiditeta, uključujući AIM, je kod obolelih od insulin-nezavisnog dijabetesa veći nego kod nedijabetičara iste životne dobi. Jedan od razloga za veći mortalitet od infarkta miokarda kod dijabetičara može biti i srčana insuficijencija. Bolesnici sa diajbetesom i AIM imaju povećan rizik od lošeg ishoda terapije AIM u odnosu na nedijabetičare, a osnovni razlozi su endotelna disfunkcija, protrombotično stanje, veća mogućnost restenoze, negativnog vaskularnog remodelovanja, povećane glikolizacije proteinai depozicije vaskularnog matriksa. U okviru ovog preglednog članka, dat je prikaz najnovijih literaturnih podataka i praktičnih saznanja o AIM kod dijabetičnih bolesnika., Acute myocardial infarction (AMI) is a clinical form of coronary heart disease, which occurs after coronary arteries' occlusion and irreversible ischemia progression leads to myocardial necrosis. Morbidity and mortality caused by cardiovascular comorbidities, including AIM, are greater in patients with insulin - dependent diabetes than in non - diabetes patients of the same age. One of the reasons for a higher mortality rate from AMI in patients with diabetes may be heart failure. In addition, patients with diabetes and AMI have an increased risk for poor therapy outcomes of AMI compared with non - diabetes patients, and the main reasons are endothelial dysfunction, prothrombotic state, a greater possibility of restenosis, negative vascular remodelling, increased protein glycosylation, and vascular matrix deposition. In this review, we provide an overview of recent literature data and practical knowledge related to the AMI in diabetic patients.",
journal = "Medicinska istraživanja",
title = "Akutni infarkt miokarda i diabetes mellitus, Acute myocardial infarction and diabetes mellitus",
volume = "49",
number = "3",
pages = "16-19",
doi = "10.5937/MedIst1503016G"
}

Gluvić, Z., Kovačević, P., Obradović, M. M., Trebaljevac, J., Samardžić, V., Lačković, M.,& Isenović, E. R.. (2015). Akutni infarkt miokarda i diabetes mellitus. in Medicinska istraživanja, 49(3), 16-19.
https://doi.org/10.5937/MedIst1503016G

Gluvić Z, Kovačević P, Obradović MM, Trebaljevac J, Samardžić V, Lačković M, Isenović ER. Akutni infarkt miokarda i diabetes mellitus. in Medicinska istraživanja. 2015;49(3):16-19.
doi:10.5937/MedIst1503016G .

Gluvić, Zoran, Kovačević, Pejka, Obradović, Milan M., Trebaljevac, Jovana, Samardžić, Vladimir, Lačković, Milena, Isenović, Esma R., "Akutni infarkt miokarda i diabetes mellitus" in Medicinska istraživanja, 49, no. 3 (2015):16-19,
https://doi.org/10.5937/MedIst1503016G . .