Evidence for altered adipocyte function in polycystic ovary syndrome

Abstract

Background: Adipocytokines are produced by adipose tissue and have been thought to be related to insulin resistance and other health consequences. We measured leptin, adiponectin, and resistin simultaneously in women with polycystic ovary syndrome (PCOS) and age-and weight-matched controls. Our hypothesis was that these simultaneous measurements would help determine whether adipocytokine secretion is abnormal in PCOS independent of body mass and whether these levels are related to insulin resistance as well as other hormonal changes. Methods: Fifty-two women with PCOS and 45 normal ovulatory women who were age-and weightmatched were studied. Blood was obtained for adipocytokines (leptin, adiponectin, and resistin) as well as hormonal parameters and markers of insulin resistance as assessed by the quantitative insulin-sensitivity check index. Body mass index (BMI) was stratified into obese, overweight, and normal subgroups for comparisons between PCOS and controls. Results: Adiponectin was lower (P , 0.05) and resistin was higher (P , 0.05) while leptin was similar to matched controls. Breakdown of the groups into subgroups showed a strong body mass relationship for leptin with no changes in resistin although adiponectin was lower in PCOS, even controlling for BMI. In controls, leptin and adiponectin and leptin and resistin correlated (P , 0.05) but not in PCOS. In controls, all adipocytokines correlated with markers of insulin resistance but not in PCOS. Conclusions: When matched for BMI status, decreased adiponectin in PCOS represent the most marked change. This alteration may be the result of altered adipose tissue distribution and function in PCOS but no correlation with insulin resistance was found.

The ‘beneficial’ adipokines in reproduction and fertility

“…44 Evidence for the effects of adiponectin on the human ovary is also derived from the observation of reduced adiponectin levels in women diagnosed with PCOS, independent of obesity. [45][46][47] Causation is less clear, as obesity and PCOS both cause hyperandrogenemia, 1,46 and adipose tissue synthesis of adiponectin is reduced by androgens. 48 Nonetheless, genomic studies support the view that hypoadiponectinemia is a causative agent in PCOS.…”

Association of PPARG Pro12Ala polymorphism with insulin sensitivity and body mass index in patients with polycystic ovary syndrome

“…Various PCOS phenotypes presumably result from the interaction between multiple predisposing genomic variants, each exerting only minor effects and strong environmental influences (2). As PCOS is associated with obesity, insulin resistance and compensatory hyperinsulinemia (3), disturbed secretion of adipokines (4) and an elevated risk for diabetes mellitus type 2 (T2DM) (5) and cardiovascular diseases (CVD) (6), the peroxisome proliferator-activated receptor gamma (PPARG) represents a strong candidate gene predisposing to PCOS.…”

Expression and effect of resistin on bovine and rat granulosa cell steroidogenesis and proliferation

“…In cultured human theca cells, 17a-hydroxylase activity is increased by resistin in the presence of forskolin or forskolinGinsulin, suggesting a role of resistin in stimulation of androgen production by theca cells (Munir et al 2005). Moreover, some studies have shown elevated concentrations of serum resistin in women with polycystic ovary syndrome (Panidis et al 2004, Carmina et al 2005, Munir et al 2005, Yilmaz et al 2009, which is known to be associated with hyperinsulinemia, hyperandrogenism, and insulin resistance (Gambineri et al 2002). In mammals, insulin as well as insulin-like growth factor 1 (IGF1) is well known to play a key role on the development of antral follicles, i.e.…”