The management of insulin resistance in polycystic ovary syndrome

Trends Endocrinol Metab. 2007 Sep;18(7):273-9. doi: 10.1016/j.tem.2007.08.001. Epub 2007 Aug 16.

Abstract

Polycystic ovary syndrome (PCOS) has reproductive and metabolic implications. Insulin resistance (IR), secondary to genetic and lifestyle factors, is integral in the pathogenesis, metabolic, clinical features and the long-term sequelae in the majority of people with PCOS. Therapeutic strategies targeting IR in PCOS ameliorate clinical features and might reduce long-term sequelae including diabetes. The mainstay for improving IR is lifestyle change; however, feasibility and sustainability remain concerns. In PCOS, metformin reduces IR, improves ovarian function, regulates cycles, lowers androgens, improves clinical hyperandrogenism and potentially improves fertility. Metformin is also likely to delay diabetes onset and has a role in PCOS in those at high risk of diabetes; however, further research is needed to clarify specific target subgroups and clinical indications.

Publication types

  • Review

MeSH terms

  • Female
  • Humans
  • Hyperinsulinism / complications
  • Hyperinsulinism / drug therapy
  • Hyperinsulinism / physiopathology
  • Hypoglycemic Agents / pharmacology
  • Hypoglycemic Agents / therapeutic use
  • Insulin Resistance*
  • Metformin / pharmacology
  • Metformin / therapeutic use
  • Models, Biological
  • Polycystic Ovary Syndrome / complications
  • Polycystic Ovary Syndrome / drug therapy*
  • Polycystic Ovary Syndrome / physiopathology*

Substances

  • Hypoglycemic Agents
  • Metformin