Insulin Resistance and Polycystic Ovary Syndrome

• Published in: Current pharmaceutical design Vol. 22; no. 36; p. 5526
• Main Author: Moghetti, Paolo
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01.01.2016
• Subjects: Animals; Female; Humans; Insulin Resistance; Polycystic Ovary Syndrome - drug therapy; Polycystic Ovary Syndrome - epidemiology; Polycystic Ovary Syndrome - metabolism; Polycystic Ovary Syndrome - physiopathology
• ISSN: 1873-4286
• DOI: 10.2174/1381612822666160720155855

Insulin resistance and the associated compensatory hyperinsulinemia are common findings in women with PCOS, and may play a key role in this condition. In this article, we focused on the significance of insulin resistance in PCOS, reviewing the available literature on epidemiology, pathogenesis, pathophysiology and treatment of this condition. It has been estimated that approximately 70% of these women are insulin resistant, but this figure is affected by frequent referral bias. In addition, there is metabolic heterogeneity between clinical phenotypes of PCOS. A fundamental issue is the role that hyperinsulinemia plays in androgen overproduction, which is enhanced by bidirectional links between insulin resistance and hyperandrogenism. Available data suggest that women with PCOS may have insulin action alterations of heterogeneous origins, which induce specific abnormalities in these subjects due to the presence of intrinsic defects. Obesity is a common finding in these patients and contributes to the association between PCOS and insulin resistance, combining with the effect of PCOS per se. Insulin sensitization shows several beneficial effects in the treatment of this condition. However, clinical response is heterogeneous. Insulin resistance is a common feature of women with PCOS, although it is not universal and differ between clinical phenotypes of PCOS. Insulin resistance and hyperandrogenism appear to be interrelated key factors in the pathogenesis of PCOS. We hypothesize that PCOS might represent a common end-stage clinical phenotype of different processes, in which there are impaired insulin action and hyperandrogenism, probably favoured by specific, intrinsic abnormalities of these women.