SFEBES2009 Oral Communications Cardiovascular metabolism (8 abstracts)
Insulin increases and metformin decreases the novel adipokine chemerin in insulin resistant subjects: PCOS as a paradigm
Bee Tan 1 , Jing Chen 1 , Raghu Adya 1 , Jaspreet Kaur 1 , Dennis Heutling 2 , Krzysztof C Lewandowski 3 , Hendrik Lehnert 2 & Harpal Randeva 1
1University of Warwick, Coventry, UK; 2University of Lübeck, Lübeck, Germany; 3The Medical University of Lodz and Polish Mother’s Memorial Research Institute, Lodz, Poland.
Adipose tissue produces several hormones and cytokines termed ‘adipokines’ that have widespread effects on carbohydrate and lipid metabolism. They appear to play an important role in the pathogenesis of insulin resistance, diabetes, and atherosclerosis. Chemerin is a novel adipokine, highly expressed in obese, insulin-resistant subjects. Polycystic ovary syndrome (PCOS) is associated with insulin resistance and obesity. We assessed chemerin levels in sera and adipose tissue from PCOS women and matched controls. In vivo and ex vivo regulation of adipose tissue chemerin by insulin as well as the effects of metformin treatment on serum chemerin levels in PCOS subjects were also studied. Real-time RT-PCR and western blotting were used to assess mRNA and protein expression of chemerin. Serum chemerin was measured by ELISA. We investigated the in vivo effects of insulin on serum chemerin levels via a prolonged insulin–glucose infusion. The ex vivo effect of insulin on adipose tissue chemerin protein production and secretion into conditioned media were assessed by western blotting and ELISA, respectively. Serum chemerin, subcutaneous and omental adipose tissue chemerin were significantly higher in PCOS women (P<0.05). Hyperinsulinemic induction in human subjects significantly increased serum chemerin levels (P<0.05). Also, in adipose tissue explants, insulin caused a significant dose-dependent increase in chemerin protein production and secretion into conditioned media (P<0.05). After 6 months of metformin treatment, there was a significant decrease in serum chemerin (P<0.01). Importantly, changes in HOMA-IR were predictive of changes in serum chemerin (P=0.046). In conclusion, serum and adipose tissue chemerin levels are increased in PCOS women and are up-regulated by insulin. Metformin treatment decreases serum chemerin in these women. Our novel findings provide perspectives into chemerin biology and highlight the role of metformin in modulating chemerin levels in insulin resistant PCOS women.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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