| Literature DB >> 33460482 |
Thomas M Barber1,2, Stephen Franks3.
Abstract
The increased global prevalence of obesity over the last 40-years has driven a rise in prevalence of obesity-related co-morbidities, including Polycystic Ovary Syndrome (PCOS). On a background of genetic susceptibility, PCOS often becomes clinically manifest following weight-gain, commonly during adolescence. A common endocrinopathy affecting between 6-10% of reproductive age women, PCOS presents with the cardinal features of hyperandrogenism, reproductive and metabolic dysfunction. PCOS associates with insulin resistance, independently of (but amplified by) obesity. Insulin resistance in PCOS is characterised by abnormal post-receptor signalling within the phosphotidylinositol-kinase (PI3-K) pathway. Multiple factors (including most notably, weight-gain) contribute towards the severity of insulin resistance in PCOS. Compensatory hyperinsulinaemia ensues, resulting in over-stimulation of the (intact) post-receptor mitogen-activated protein kinase (MAP-K) insulin pathway, with consequent implications for steroidogenesis and ovarian function. In this concise review, we explore the effects of weight gain and obesity on the pathogenesis of PCOS from the perspective of its three cardinal features of hyperandrogenism, reproductive and metabolic dysfunction, with a focus on the central mediating role of the insulin pathway. We also consider key lifestyle strategies for the effective management of obese and overweight women with PCOS. This article is protected by copyright. All rights reserved.Entities:
Keywords: Metabolism; Obesity; Polycystic Ovary Syndrome
Year: 2021 PMID: 33460482 DOI: 10.1111/cen.14421
Source DB: PubMed Journal: Clin Endocrinol (Oxf) ISSN: 0300-0664 Impact factor: 3.478