Background: Polycystic ovary syndrome (PCOS) is a com-mon endocrine and metabolic disease, occurring in 2.2–10% of adolescence and childbearing age women. Clinical and/or bio-chemical hyperandrogenism is an important feature of PCOS. Adipose tissue is not only an energy storage organ, but also the largest endocrine organ, playing an important role in energy balance, reproductive function maintenance and steroid storage and metabolism. The increasing epidemic of
PCOS has led to a great deal of interest in the function of adipose tissue (AT) and dysfunction of AT has been involved in the pathogenesis of PCOS. The enzyme 11BHSD1 catalyzes the regeneration of active cortisol from inert cortisone while 11BHSD2 partici-pates in inactivating cortisol to cortisone. Although attention has focused on local sources of cortisol and, in particular, on the AT expression of 11BHSD-1, very limited information ex-ists on expression of 11BHSD-1 and 11BHSD2 in AT of
PCOS women. Thus our objective was to assess mRNA abundance of 11BHSD1 and 11BHSD2 in abdominal subcutaneous AT of pregnant women with
PCOS and also non-PCOS pregnant women at delivery day.Materials and Methods: In this case control study, signed informed consent was obtained from all subjects, abdominal subcutaneous AT samples (3-4 g) from 13 pregnant women with
PCOS and 13 pregnant non-PCOS women were collected during cesarean section. Samples were stored at liquid nitrogen (-196 °C) until analysis. 11BHSD1, 2 genes expression were measured by real time qPCR technique.Results: The level of mRNA expression of 11BHSD1and 11BHSD2 did not differ significantly between two groups (P> 0.05). The level of mRNA expression of 11BHSD1 was lower in
PCOS subjects and 11BHSD2 expression level in
PCOS group was higher. Also, no significant differences were found with respect to age and body mass index before preg-nancy and at delivery day among non-PCOS and
PCOS AT.Conclusion: Based on our data it can be hypothesized that low-er expression of 11BHSD1 lead to less conversion of cortison to cortisol in
PCOS that may amplify cortison accumulation in AT of
PCOS than non-PCOS women. Further studies are warranted to replicate these findings as well as investigate gene expression profiles in lager sample size.