Induction of hyperandrogenism in lean reproductive-age women stimulates proatherogenic inflammation

F. González, K. Sreekumaran Nair, E. Basal, D. M. Bearson, J. M. Schimke, H. E. Blair

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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 130mg 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 2h 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.

Original languageEnglish
Pages (from-to)439-444
Number of pages6
JournalHormone and Metabolic Research
Volume47
Issue number6
DOIs
StatePublished - Sep 17 2014

Fingerprint

Hyperandrogenism
Interleukin-6
Fasting
Inflammation
Glucose
Eating
Polycystic Ovary Syndrome
Placebos
Matrix Metalloproteinases
C-Reactive Protein
Androgens
Plasmas
Messenger RNA
Androstenedione
Matrix Metalloproteinase 2
Plasma Cells
Sulfates
Testosterone
Proteins
Chemical activation

Keywords

  • atherogenesis
  • hyperglycemia
  • inflammation

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism

Cite this

González, F., Sreekumaran Nair, K., Basal, E., Bearson, D. M., Schimke, J. M., & Blair, H. E. (2014). Induction of hyperandrogenism in lean reproductive-age women stimulates proatherogenic inflammation. Hormone and Metabolic Research, 47(6), 439-444. https://doi.org/10.1055/s-0034-1387791

Induction of hyperandrogenism in lean reproductive-age women stimulates proatherogenic inflammation. / González, F.; Sreekumaran Nair, K.; Basal, E.; Bearson, D. M.; Schimke, J. M.; Blair, H. E.

In: Hormone and Metabolic Research, Vol. 47, No. 6, 17.09.2014, p. 439-444.

Research output: Contribution to journalArticle

González, F, Sreekumaran Nair, K, Basal, E, Bearson, DM, Schimke, JM & Blair, HE 2014, 'Induction of hyperandrogenism in lean reproductive-age women stimulates proatherogenic inflammation', Hormone and Metabolic Research, vol. 47, no. 6, pp. 439-444. https://doi.org/10.1055/s-0034-1387791
González, F. ; Sreekumaran Nair, K. ; Basal, E. ; Bearson, D. M. ; Schimke, J. M. ; Blair, H. E. / Induction of hyperandrogenism in lean reproductive-age women stimulates proatherogenic inflammation. In: Hormone and Metabolic Research. 2014 ; Vol. 47, No. 6. pp. 439-444.
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