Bozic-Antic, Ivana

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  • Bozic-Antic, Ivana (2)
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Author's Bibliography

Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome

Tepavčević, Snežana; Milutinovic, Danijela Vojnovic; Macut, Djuro; Stojiljković, Mojca D.; Nikolic, Marina; Bozic-Antic, Ivana; Ćulafić, Tijana; Bjekic-Macut, Jelica; Matić, Gordana; Korićanac, Goran

(2015)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, Danijela Vojnovic
AU  - Macut, Djuro
AU  - Stojiljković, Mojca D.
AU  - Nikolic, Marina
AU  - Bozic-Antic, Ivana
AU  - Ćulafić, Tijana
AU  - Bjekic-Macut, Jelica
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/710
AB  - Polycystic ovary syndrome (PCOS) is associated with an altered plasma lipid profile and increased risk for cardiovascular diseases. We hypothesized that molecular mechanisms underlying cardiac pathology in PCOS involve changes in expression and subcellular localization of several key proteins involved in cardiac lipid transport and metabolism, such as fatty acid transporter CD36, lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1), and carnitine palmitoyltransferase 1 (CPT1). We used the animal model of PCOS obtained by treating female rats with dihydrotestosterone (DHT). Protein levels of CD36, lipin 1, PPAR alpha, PGC1, and antioxidative enzymes were assessed by Western blot in different cardiac cell compartments. Cardiac triglycerides (TG) and lipid peroxidation were also measured. The content of CD36 was decreased in both the cardiac plasma membranes and intracellular pool. On the other hand, total content of cardiac lipin 1 in DHT-treated rats was elevated, in contrast to decreased microsomal lipin 1 content. An increase in nuclear content of lipin 1 was observed together with elevation of nuclear PPAR alpha and PGC1, and an increase in CPT1 expression. However, lipid peroxidation was reduced in the heart, without alterations in antioxidative enzymes expression and cardiac TG content. The results indicate that treatment of female rats with DHT is accompanied by a decrease of fatty acid uptake and a reduction of lipid peroxidation in the heart. The observed elevation of lipin 1, PPAR alpha, PGC1, and CPT1 expression suggests that cardiac fatty acid metabolism is shifted toward mitochondrial beta oxidation.
T2  - Endocrine
T1  - Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome
VL  - 50
IS  - 1
SP  - 193
EP  - 201
DO  - 10.1007/s12020-015-0558-1
ER  - 
@article{
author = "Tepavčević, Snežana and Milutinovic, Danijela Vojnovic and Macut, Djuro and Stojiljković, Mojca D. and Nikolic, Marina and Bozic-Antic, Ivana and Ćulafić, Tijana and Bjekic-Macut, Jelica and Matić, Gordana and Korićanac, Goran",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/710",
abstract = "Polycystic ovary syndrome (PCOS) is associated with an altered plasma lipid profile and increased risk for cardiovascular diseases. We hypothesized that molecular mechanisms underlying cardiac pathology in PCOS involve changes in expression and subcellular localization of several key proteins involved in cardiac lipid transport and metabolism, such as fatty acid transporter CD36, lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1), and carnitine palmitoyltransferase 1 (CPT1). We used the animal model of PCOS obtained by treating female rats with dihydrotestosterone (DHT). Protein levels of CD36, lipin 1, PPAR alpha, PGC1, and antioxidative enzymes were assessed by Western blot in different cardiac cell compartments. Cardiac triglycerides (TG) and lipid peroxidation were also measured. The content of CD36 was decreased in both the cardiac plasma membranes and intracellular pool. On the other hand, total content of cardiac lipin 1 in DHT-treated rats was elevated, in contrast to decreased microsomal lipin 1 content. An increase in nuclear content of lipin 1 was observed together with elevation of nuclear PPAR alpha and PGC1, and an increase in CPT1 expression. However, lipid peroxidation was reduced in the heart, without alterations in antioxidative enzymes expression and cardiac TG content. The results indicate that treatment of female rats with DHT is accompanied by a decrease of fatty acid uptake and a reduction of lipid peroxidation in the heart. The observed elevation of lipin 1, PPAR alpha, PGC1, and CPT1 expression suggests that cardiac fatty acid metabolism is shifted toward mitochondrial beta oxidation.",
journal = "Endocrine",
title = "Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome",
volume = "50",
number = "1",
pages = "193-201",
doi = "10.1007/s12020-015-0558-1"
}
Tepavčević, S., Milutinovic, D. V., Macut, D., Stojiljković, M. D., Nikolic, M., Bozic-Antic, I., Ćulafić, T., Bjekic-Macut, J., Matić, G.,& Korićanac, G. (2015). Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome.
Endocrine, 50(1), 193-201.
https://doi.org/10.1007/s12020-015-0558-1
Tepavčević S, Milutinovic DV, Macut D, Stojiljković MD, Nikolic M, Bozic-Antic I, Ćulafić T, Bjekic-Macut J, Matić G, Korićanac G. Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome. Endocrine. 2015;50(1):193-201
Tepavčević Snežana, Milutinovic Danijela Vojnovic, Macut Djuro, Stojiljković Mojca D., Nikolic Marina, Bozic-Antic Ivana, Ćulafić Tijana, Bjekic-Macut Jelica, Matić Gordana, Korićanac Goran, "Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome" Endocrine, 50, no. 1 (2015):193-201,
https://doi.org/10.1007/s12020-015-0558-1 .
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Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome

Tepavčević, Snežana; Milutinovic, Danijela Vojnovic; Macut, Djuro; Žakula, Zorica; Nikolic, Marina; Bozic-Antic, Ivana; Romić, Snježana Đ.; Bjekic-Macut, Jelica; Matić, Gordana; Korićanac, Goran

(2014)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, Danijela Vojnovic
AU  - Macut, Djuro
AU  - Žakula, Zorica
AU  - Nikolic, Marina
AU  - Bozic-Antic, Ivana
AU  - Romić, Snježana Đ.
AU  - Bjekic-Macut, Jelica
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5970
AB  - It is supposed that women with polycystic ovary syndrome (PCOS) are prone to develop cardiovascular disease as a consequence of multiple risk factors that are mostly related to the state of insulin resistance and consequent hyperinsulinemia. In the present study, we evaluated insulin signaling and glucose transporters (GLUT) in cardiac cells of dihydrotestosterone (DHT) treated female rats as an animal model of PCOS. Expression of proteins involved in cardiac insulin signaling pathways and glucose transporters, as well as their phosphorylation or intracellular localization were studied by Western blot analysis in DHT-treated and control rats. Treatment with DHT resulted in increased body mass, absolute mass of the heart, elevated plasma insulin concentration, dyslipidemia and insulin resistance. At the molecular level, DHT treatment did not change protein expression of cardiac insulin receptor and insulin receptor substrate 1, while phosphorylation of the substrate at serine 307 was increased. Unexpectedly, although expression of downstream Akt kinase and its phosphorylation at threonine 308 were not altered, phosphoiylation of Akt at serine 473 was increased in the heart of DHT-treated rats. In contrast, expression and phosphorylation of extracellular signal regulated kinases 1/2 were decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased, as well as the expression of GLUT4 in cardiac cells at the end of androgen treatment. The obtained results provide evidence for alterations in expression and especially in functional characteristics of insulin signaling molecules and glucose transporters in the heart of DHT-treated rats with PCOS, indicating impaired cardiac insulin action. (c) 2014 Elsevier Ltd. All rights reserved.
T2  - Journal of Steroid Biochemistry and Molecular Biology
T1  - Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome
VL  - 141
SP  - 71
EP  - 76
DO  - 10.1016/j.jsbmb.2014.01.006
ER  - 
@article{
author = "Tepavčević, Snežana and Milutinovic, Danijela Vojnovic and Macut, Djuro and Žakula, Zorica and Nikolic, Marina and Bozic-Antic, Ivana and Romić, Snježana Đ. and Bjekic-Macut, Jelica and Matić, Gordana and Korićanac, Goran",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5970",
abstract = "It is supposed that women with polycystic ovary syndrome (PCOS) are prone to develop cardiovascular disease as a consequence of multiple risk factors that are mostly related to the state of insulin resistance and consequent hyperinsulinemia. In the present study, we evaluated insulin signaling and glucose transporters (GLUT) in cardiac cells of dihydrotestosterone (DHT) treated female rats as an animal model of PCOS. Expression of proteins involved in cardiac insulin signaling pathways and glucose transporters, as well as their phosphorylation or intracellular localization were studied by Western blot analysis in DHT-treated and control rats. Treatment with DHT resulted in increased body mass, absolute mass of the heart, elevated plasma insulin concentration, dyslipidemia and insulin resistance. At the molecular level, DHT treatment did not change protein expression of cardiac insulin receptor and insulin receptor substrate 1, while phosphorylation of the substrate at serine 307 was increased. Unexpectedly, although expression of downstream Akt kinase and its phosphorylation at threonine 308 were not altered, phosphoiylation of Akt at serine 473 was increased in the heart of DHT-treated rats. In contrast, expression and phosphorylation of extracellular signal regulated kinases 1/2 were decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased, as well as the expression of GLUT4 in cardiac cells at the end of androgen treatment. The obtained results provide evidence for alterations in expression and especially in functional characteristics of insulin signaling molecules and glucose transporters in the heart of DHT-treated rats with PCOS, indicating impaired cardiac insulin action. (c) 2014 Elsevier Ltd. All rights reserved.",
journal = "Journal of Steroid Biochemistry and Molecular Biology",
title = "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome",
volume = "141",
pages = "71-76",
doi = "10.1016/j.jsbmb.2014.01.006"
}
Tepavčević, S., Milutinovic, D. V., Macut, D., Žakula, Z., Nikolic, M., Bozic-Antic, I., Romić, S. Đ., Bjekic-Macut, J., Matić, G.,& Korićanac, G. (2014). Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome.
Journal of Steroid Biochemistry and Molecular Biology, 141, 71-76.
https://doi.org/10.1016/j.jsbmb.2014.01.006
Tepavčević S, Milutinovic DV, Macut D, Žakula Z, Nikolic M, Bozic-Antic I, Romić SĐ, Bjekic-Macut J, Matić G, Korićanac G. Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome. Journal of Steroid Biochemistry and Molecular Biology. 2014;141:71-76
Tepavčević Snežana, Milutinovic Danijela Vojnovic, Macut Djuro, Žakula Zorica, Nikolic Marina, Bozic-Antic Ivana, Romić Snježana Đ., Bjekic-Macut Jelica, Matić Gordana, Korićanac Goran, "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome" Journal of Steroid Biochemistry and Molecular Biology, 141 (2014):71-76,
https://doi.org/10.1016/j.jsbmb.2014.01.006 .
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