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Horm Metab Res 2015; 47(06): 439-444
DOI: 10.1055/s-0034-1387791
Endocrine Care
© Georg Thieme Verlag KG Stuttgart · New York

Induction of Hyperandrogenism in Lean Reproductive-Age Women Stimulates Proatherogenic Inflammation

F. González
1   Department of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, Indiana, USA
,
K. Sreekumaran Nair
2   Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA
,
E. Basal
3   Department of Obstetrics and Gynecology, Mayo Clinic, Rochester, Minnesota, USA
,
D. M. Bearson
4   Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA
,
J. M. Schimke
2   Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA
,
H. E. Blair
4   Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA
› Author Affiliations
Further Information

Publication History

received 01 July 2014

accepted 05 August 2014

Publication Date:
17 September 2014 (online)

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Abstract

We determined the effect of hyperandrogenemia as observed in polycystic ovary syndrome (PCOS) on fasting and glucose-stimulated proatherogenic inflammation markers in lean healthy reproductive-age women. Sixteen lean healthy ovulatory reproductive-age women were treated with 130 mg of DHEA or placebo (n=8 each) for 5 days. Interleukin-6 (IL-6) mRNA and IL-6 release from mononuclear cells (MNC), plasma IL-6 and C-reactive protein (CRP), and MNC-derived (matrix metalloproteinase-2) MMP-2 protein were quantified in the fasting state and 2 h after glucose ingestion, before and after treatment. Before treatment, subjects receiving dehydroepinadrosterone (DHEA) or placebo exhibited no differences in androgens, or any proatherogenic inflammation markers while fasting and after glucose ingestion. Compared with placebo, DHEA administration raised levels of testosterone, androstenedione, and DHEA-sulfate (DHEA-S), and increased the percent change from baseline in fasting IL-6 mRNA, IL-6 release, plasma IL-6, and CRP and MMP-2 protein. However, there were no differences in any of the proatherogenic inflammation markers following glucose ingestion after DHEA administration. We conclude that in lean reproductive-age women, proatherogenic inflammation in the fasting state increases after raising circulating androgens to levels observed in PCOS. However, this hyperandrogenemia-induced MNC activation does not provoke a similar response to subsequent glucose ingestion.

Key words

atherogenesis - inflammation - hyperglycemia
 

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