TY  - JOUR
AU  - Tepavcevic, Snezana
AU  - Vojnović-Milutinović, Danijela
AU  - Macut, Djuro
AU  - Stojiljkovic, Mojca
AU  - Radovanović, Marina
AU  - Bozic-Antic, Ivana
AU  - Culafic, Tijana
AU  - Bjekić-Macut, Jelica
AU  - Matić, Gordana
AU  - Koricanac, Goran
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1911
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
IS  - 1
VL  - 50
DO  - 10.1007/s12020-015-0558-1
SP  - 193
EP  - 201
ER  - 

@article{
author = "Tepavcevic, Snezana and Vojnović-Milutinović, Danijela and Macut, Djuro and Stojiljkovic, Mojca and Radovanović, Marina and Bozic-Antic, Ivana and Culafic, Tijana and Bjekić-Macut, Jelica and Matić, Gordana and Koricanac, Goran",
year = "2015",
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",
number = "1",
volume = "50",
doi = "10.1007/s12020-015-0558-1",
pages = "193-201"
}

Tepavcevic, S., Vojnović-Milutinović, D., Macut, D., Stojiljkovic, M., Radovanović, M., Bozic-Antic, I., Culafic, T., Bjekić-Macut, J., Matić, G.,& Koricanac, G.. (2015). Cardiac fatty acid uptake and metabolism in the rat model of polycystic
 ovary syndrome. in Endocrine, 50(1), 193-201.
https://doi.org/10.1007/s12020-015-0558-1

Tepavcevic S, Vojnović-Milutinović D, Macut D, Stojiljkovic M, Radovanović M, Bozic-Antic I, Culafic T, Bjekić-Macut J, Matić G, Koricanac G. Cardiac fatty acid uptake and metabolism in the rat model of polycystic
 ovary syndrome. in Endocrine. 2015;50(1):193-201.
doi:10.1007/s12020-015-0558-1 .

Tepavcevic, Snezana, Vojnović-Milutinović, Danijela, Macut, Djuro, Stojiljkovic, Mojca, Radovanović, Marina, Bozic-Antic, Ivana, Culafic, Tijana, Bjekić-Macut, Jelica, Matić, Gordana, Koricanac, Goran, "Cardiac fatty acid uptake and metabolism in the rat model of polycystic
 ovary syndrome" in Endocrine, 50, no. 1 (2015):193-201,
https://doi.org/10.1007/s12020-015-0558-1 . .

TY  - JOUR
AU  - Tepavcevic, Snezana
AU  - Vojnović-Milutinović, Danijela
AU  - Macut, Djuro
AU  - Zakula, Zorica
AU  - Radovanović, Marina
AU  - Bozic-Antic, Ivana
AU  - Romic, Snjezana
AU  - Bjekić-Macut, Jelica
AU  - Matić, Gordana
AU  - Koricanac, Goran
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2217
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
DO  - 10.1016/j.jsbmb.2014.01.006
SP  - 71
EP  - 76
ER  - 

@article{
author = "Tepavcevic, Snezana and Vojnović-Milutinović, Danijela and Macut, Djuro and Zakula, Zorica and Radovanović, Marina and Bozic-Antic, Ivana and Romic, Snjezana and Bjekić-Macut, Jelica and Matić, Gordana and Koricanac, Goran",
year = "2014",
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",
doi = "10.1016/j.jsbmb.2014.01.006",
pages = "71-76"
}

Tepavcevic, S., Vojnović-Milutinović, D., Macut, D., Zakula, Z., Radovanović, M., Bozic-Antic, I., Romic, S., Bjekić-Macut, J., Matić, G.,& Koricanac, G.. (2014). Dihydrotestosterone deteriorates cardiac insulin signaling and glucose
 transport in the rat model of polycystic ovary syndrome. in Journal of Steroid Biochemistry and Molecular Biology, 141, 71-76.
https://doi.org/10.1016/j.jsbmb.2014.01.006

Tepavcevic S, Vojnović-Milutinović D, Macut D, Zakula Z, Radovanović M, Bozic-Antic I, Romic S, Bjekić-Macut J, Matić G, Koricanac G. Dihydrotestosterone deteriorates cardiac insulin signaling and glucose
 transport in the rat model of polycystic ovary syndrome. in Journal of Steroid Biochemistry and Molecular Biology. 2014;141:71-76.
doi:10.1016/j.jsbmb.2014.01.006 .

Tepavcevic, Snezana, Vojnović-Milutinović, Danijela, Macut, Djuro, Zakula, Zorica, Radovanović, Marina, Bozic-Antic, Ivana, Romic, Snjezana, Bjekić-Macut, Jelica, Matić, Gordana, Koricanac, Goran, "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose
 transport in the rat model of polycystic ovary syndrome" in Journal of Steroid Biochemistry and Molecular Biology, 141 (2014):71-76,
https://doi.org/10.1016/j.jsbmb.2014.01.006 . .