Review

The contribution of hyperinsulinemia to the hyperandrogenism of polycystic ovary syndrome

Nadia B. Pateguana, Alvin Janes
Journal of Metabolic Health | Journal of Insulin Resistance: Vol 4, No 1, | a50 | DOI: https://doi.org/10.4102/jir.v4i1.50 | © 2019 Nadia B. Pateguana, Alvin Janes | This work is licensed under CC Attribution 4.0
Submitted: 16 May 2019 | Published: 02 July 2019

About the author(s)

Nadia B. Pateguana, Intensive Dietary Management Program, Toronto, Canada
Alvin Janes, Faculty of Medicine, University of Manitoba, Winnipeg, Canada

Abstract

Background: Polycystic Ovary Syndrome (PCOS) is a very common endocrine disorder of young women.

Aim: The proper treatment of PCOS requires a thorough understanding of the underlying cause of disease. In this article, we review the extent to which hyperinsulinemia contributes to the development of PCOS.

Setting: The goal of this review was to assess the current literature on the contribution of hyperinsulinemia to the hyperandrogenism of polycystic ovary syndrome in hopes of promoting future research and advancements in clinical treatments for women with PCOS focusing on this major contributing factor, hyperinsulinemia.

Method: A review of published peer-reviewed literature was conducted by searching the keywords.

Results: Excessive insulin causes both the overproduction of testosterone and decreased sex hormone binding globulin (SHBG) levels seen in PCOS, both of which collaborate in creating an increased testosterone effect.

Conclusion: The majority of research and evidence shows that the hyperandrogenism of PCOS is likely caused by hyperinsulinemia. Yet the conventional treatment of hyperandrogenic symptoms in women with PCOS is not directed towards correcting this underlying hyperinsulinemia. Further research is needed to assess how the treatment of the hyperinsulinemia through lifestyle would compare to the current treatment of hyperandrogenemia through testosterone-lowering drugs.


Keywords

PCOS; hyperandrogenemia; hyperinsulinemia; fertility; insulin resistance

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