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Updated: Apr 27, 2026

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome

Published on: October 2, 2018

DHEA, DHEAS and PCOS.

Mark O Goodarzi¹, Enrico Carmina², Ricardo Azziz³

¹Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.

The Journal of Steroid Biochemistry and Molecular Biology

|July 11, 2014

Summary

This summary is machine-generated.

Excess adrenal precursor androgen (APA) production, marked by DHEAS, is seen in 20-30% of PCOS patients. This excess likely stems from an inherited exaggeration in androgen biosynthesis, though its exact cause in PCOS remains unclear.

Keywords:

Adrenal Androgens Dehydroepiandrosterone (DHEA)Dehydroepiandrosterone sulfate (DHEAS)Genetics Polycystic ovary syndrome

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Published on: July 5, 2024

Area of Science:

Endocrinology
Reproductive Medicine
Genetics

Background:

Polycystic ovary syndrome (PCOS) affects 20-30% of women with excess adrenal precursor androgen (APA) production, often indicated by dehydroepiandrosterone sulfate (DHEAS).
While the exact role of APA excess in PCOS etiology is debated, conditions like congenital adrenal hyperplasia with APA excess can manifest a PCOS-like phenotype.
Inherited enzyme defects or cortisol metabolism issues explain only a small fraction of hyperandrogenism cases in women.

Purpose of the Study:

To investigate the origins and characteristics of excess adrenal precursor androgen (APA) production in women with PCOS.
To clarify the relationship between APA excess and the PCOS phenotype.
To explore the genetic and hormonal factors contributing to elevated APAs in PCOS.

Main Methods:

Analysis of adrenal steroidogenesis in response to ACTH stimulation in PCOS women with APA excess.
Assessment of the influence of extra-adrenal factors (obesity, insulin, ovarian secretions) on APA production.
Examination of the heritability of APAs (DHEAS) in the general population and PCOS cohorts, including genetic analyses (SNPs).

Main Results:

Women with PCOS and APA excess exhibit a generalized exaggeration in adrenal steroidogenesis upon ACTH stimulation, without overt HPA axis dysfunction.
Extra-adrenal factors like obesity and insulin resistance play a limited role in elevated APA production in PCOS.
Significant heritability of APAs (especially DHEAS) is observed, but identified SNPs explain only a small portion of this inheritance.

Conclusions:

The precise cause of APA excess in PCOS remains elusive.
APA excess in PCOS may represent a generalized, inherited exaggeration in androgen biosynthesis.
Elevated DHEAS, while potentially protective against cardiovascular risk in men and women, has an unknown role in modulating this risk specifically within the PCOS population.