Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/4002
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dc.contributor.authorTepavčević, Snežanaen_US
dc.contributor.authorMilutinović, Danijela Vojnovićen_US
dc.contributor.authorMacut, Djuroen_US
dc.contributor.authorStojiljković, Mojcaen_US
dc.contributor.authorNikolić, Marinaen_US
dc.contributor.authorBožić-Antić, Ivanaen_US
dc.contributor.authorĆulafić, Tijanaen_US
dc.contributor.authorBjekić-Macut, Jelicaen_US
dc.contributor.authorMatić, Gordanaen_US
dc.contributor.authorKorićanac, Goranen_US
dc.date.accessioned2021-04-16T15:36:38Z-
dc.date.available2021-04-16T15:36:38Z-
dc.date.issued2015-
dc.identifier.issn1355-008X-
dc.identifier.issn1559-0100-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/4002-
dc.description.abstractPolycystic 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 α (PPARα), peroxisome proliferator-activated receptor γ 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, PPARα, 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 PPARα 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, PPARα, PGC1, and CPT1 expression suggests that cardiac fatty acid metabolism is shifted toward mitochondrial beta oxidation.en_US
dc.language.isoenen_US
dc.relation.ispartofEndocrineen_US
dc.relation.ispartofseries50;193-201-
dc.subjectPolycystic ovary syndromeen_US
dc.subjectHearten_US
dc.subjectFatty acid transporten_US
dc.subjectFatty acid oxidationen_US
dc.subjectCardiac triglyceridesen_US
dc.titleCardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndromeen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s12020-015-0558-1-
dc.identifier.pmid25702158-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.fulltextWith Fulltext-
item.grantfulltextrestricted-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptChair of Biochemistry and Molecular Biology-
crisitem.author.orcid0000-0002-0142-1056-
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