SFEBES2016 Poster Presentations Reproduction (33 abstracts)
Alterations of specific caveolin isoforms in the rat uterus under insulin resistance and hyperandrogenism conditions: does metformin contributes to their regulation?
Min Hu 1 , Yuehui Zhang 2 , Xue Sun 2 , Xiaoyan Sun 2 , Fanci Meng 2 , Ruijin Shao 1 & Håkan Billig 1
1University of Gothenburg, Gothenburg, Sweden; 2Heilongjiang University of Chinese Medicine, Harbin, China.
The caveolin (CAV) consists of three isoforms (CAV1, CAV2, and CAV3) and contributes to insulin-regulated glucose metabolism. It has been reported that decreased caveolin-1 phosphorylation in the endometrium is linked with insulin resistant state in women with polycystic ovary syndrome (PCOS). Because PCOS patients often display hyperandrogenism, whether hyperandrogenism in addition to insulin resistant is involved in the regulation of caveolin expression and activation in the uterus remain unknown. In this study, we treated female rats with insulin alone or in combination with human chorionic gonadotropin (hCG), and showed that insulin resistance and hyperandrogenism change the different caveolin isoform expression in the uterus, especially in smooth muscle cells. While no significant difference in CAV1 expression was detected in all groups, we found that CAV1 (Tyr14) phosphorylation was increased in hCG-treated uterus. Further, we showed that CAV2 expression was lower in insulin-, hCG- and insulin+hCG-treated uterus than control uterus, and CAV3 expression was decreased in insulin- and hCG-treated uterus. Treatment with metformin, an insulin-sensitizer, is reported to decrease circulating insulin and androgen levels, and reduce insulin resistance in most women with PCOS. In parallel to the improvement of insulin resistance and reduction of androgen synthesis, we observed that treatment with metformin reduced CAV2 expression but not CAV1/3 expression and CAV1 (Tyr14) phosphorylation in insulin+hCG-treated uterus. Our results suggest that specific caveolin isoforms and their regulation may be influenced by the environment of insulin resistance and hyperandrogenism in the rat uterus.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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