PMOS / PCOS Pathophysiology

Current concepts in the polycystic ovary syndrome

Dunaif A, Thomas A

Published February 13, 2001 Annual Review of Medicine, 52(1), 401-419
DOI 10.1146/annurev.med.52.1.401 PMID 11160786

Abstract

Over the past 20 years, it has been clearly documented that the polycystic ovary syndrome (PCOS) has major metabolic sequelae related to insulin resistance and that insulin resistance plays an important role in the pathogenesis of the reproductive disturbances of the disorder. Family studies have indicated a genetic susceptibility to PCOS. Polycystic ovaries and hyperandrogenemia are present in approximately 50% of sisters of affected women. Increased androgen secretion and insulin resistance persist in cultured theca cells and skin fibroblasts, respectively, from women with PCOS; this finding suggests that these are intrinsic, presumably genetic, defects. Insulin resistance and elevated low-density lipoprotein (LDL) levels also cluster in the sisters of women with PCOS, consistent with genetic traits. Moreover, the brothers of women with PCOS have insulin resistance and elevated dehydroepiandrosterone sulfate (DHEAS) levels, which supports a genetic basis for these findings. Family-based studies of linkage and association have implicated several genes in the pathogenesis of PCOS. The strongest evidence to date points to a gene in the region of the insulin receptor. Insulin-sensitizing therapy mitigates the reproductive disturbances of PCOS.

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PMOS / PCOS › Pathophysiology › Insulin Resistance · Reproductive Endocrinology › Ovarian Hormones › Androgens · Menstrual Cycle › Cycle Disorders › Ovulatory Disturbances
Andrea Dunaif, Abraham Thomas
A Dunaif, A Thomas
PMID 11160786 11160786 DOI 10.1146/annurev.med.52.1.401 10.1146/annurev.med.52.1.401 Dunaif et al. 2001, Dunaif 2001