Role of hyperinsulinemia in the pathogenesis of the polycystic ovary syndrome, and its clinical implications

Semin Reprod Endocrinol. 1997 May;15(2):111-22. doi: 10.1055/s-2007-1016294.

Abstract

The polycystic ovary syndrome (PCOS) is a prevalent disorder affecting approximately 6% of women of reproductive age, and is characterized by anovulation and hyperandrogenism. It has also become apparent that a frequent feature of women with PCOS is insulin resistance accompanied by compensatory hyperinsulinemia, and increasing evidence suggests that hyperinsulinemia plays an important role in the pathogenesis of PCOS. This article will review (1) evidence indicating that insulin contributes to the hyperandrogenism of PCOS by stimulating ovarian androgen production and decreasing serum sex hormone-binding globulin (SHBG) concentrations; (2) possible direct effects of hyperinsulinemia on folliculogenesis; (3) the relationship between insulin and adrenal androgens in women; and (4) therapeutic and clinical implications of these findings.

Publication types

  • Review

MeSH terms

  • Adrenal Glands / physiopathology
  • Androgens / biosynthesis
  • Androgens / blood
  • Anovulation
  • Chromans / therapeutic use
  • Diazoxide / pharmacology
  • Female
  • Humans
  • Hyperinsulinism*
  • Hypoglycemic Agents / therapeutic use
  • Insulin / physiology
  • Insulin Resistance
  • Metformin / therapeutic use
  • Ovary / metabolism
  • Polycystic Ovary Syndrome / epidemiology
  • Polycystic Ovary Syndrome / physiopathology*
  • Polycystic Ovary Syndrome / therapy
  • Steroid 17-alpha-Hydroxylase / metabolism
  • Thiazoles / therapeutic use
  • Thiazolidinediones*
  • Troglitazone

Substances

  • Androgens
  • Chromans
  • Hypoglycemic Agents
  • Insulin
  • Thiazoles
  • Thiazolidinediones
  • Metformin
  • Steroid 17-alpha-Hydroxylase
  • Troglitazone
  • Diazoxide