作者: JunWei Qu , Yong Wang , Xiaoke Wu , Lei Gao , Lihui Hou
DOI: 10.1016/J.FERTNSTERT.2008.02.167
关键词:
摘要: Objective To investigate whether insulin resistance (IR) within theca cells may directly contribute to their hyperandrogenism, a heritable trait of polycystic ovary syndrome (PCOS). Design In vitro cell model. Setting University-affiliated laboratory. Animal(s) Porcine ovaries. Intervention(s) Ovarian from porcine follicles were isolated and cultured. Insulin was induced in without (Con) or with dexamethasone (Dex); further treated by troglitazone (Tro) metformin (Met) IR vehicle only Con cells. Main Outcome Measure(s) Medium glucose T levels; reverse transcriptase polymerase chain reaction (RT-PCR) Western blot for signal molecules androgenic enzyme. Result(s) As compared cells, Dex-treated had significantly lower [ 3 H]-glucose uptake (565 ± 58 cpm/10 6 vs. 1077 78 ) but higher medium levels (16.31 0.39 nmol/L 10.62 1.02 nmol/L) approximately twofold (0.82 0.20 μg/L 0.38±0.08μg/L). Troglitazone Met reduced the testosterone concentrations comparable those The RT-PCR showed that two sensitizers different ways reversed altered messenger RNA protein expression receptor substrate-1, transporter-4, peroxisome proliferator-activated receptor-γ, 17α-hydroxylase Dex-induced Conclusion(s) Dex could exaggerate potential suggesting possible involvement this ovarian metabolic phenotype PCOS hyperandrogenism.