Inflammation in Polycystic Ovary Syndrome

Underpinning of insulin resistance and ovarian dysfunction

Frank González

Research output: Contribution to journalArticle

113 Citations (Scopus)

Abstract

Chronic low-grade inflammation has emerged as a key contributor to the pathogenesis of Polycystic Ovary Syndrome (PCOS). A dietary trigger such as glucose is capable of inciting oxidative stress and an inflammatory response from mononuclear cells (MNC) of women with PCOS, and this phenomenon is independent of obesity. This is important because MNC-derived macrophages are the primary source of cytokine production in excess adipose tissue, and also promote adipocyte cytokine production in a paracrine fashion. The proinflammatory cytokine tumor necrosis factor-α (TNFα) is a known mediator of insulin resistance. Glucose-stimulated TNFα release from MNC along with molecular markers of inflammation are associated with insulin resistance in PCOS. Hyperandrogenism is capable of activating MNC in the fasting state, thereby increasing MNC sensitivity to glucose; and this may be a potential mechanism for promoting diet-induced inflammation in PCOS. Increased abdominal adiposity is prevalent across all weight classes in PCOS, and this inflamed adipose tissue contributes to the inflammatory load in the disorder. Nevertheless, glucose ingestion incites oxidative stress in normal weight women with PCOS even in the absence of increased abdominal adiposity. In PCOS, markers of oxidative stress and inflammation are highly correlated with circulating androgens. Chronic suppression of ovarian androgen production does not ameliorate inflammation in normal weight women with the disorder. Furthermore, in vitro studies have demonstrated the ability of pro-inflammatory stimuli to upregulate the ovarian theca cell steroidogenic enzyme responsible for androgen production. These findings support the contention that inflammation directly stimulates the polycystic ovary to produce androgens.

Original languageEnglish
Pages (from-to)300-305
Number of pages6
JournalSteroids
Volume77
Issue number4
DOIs
StatePublished - Mar 10 2012

Fingerprint

Polycystic Ovary Syndrome
Androgens
Oxidative stress
Insulin Resistance
Insulin
Inflammation
Glucose
Cytokines
Tumor Necrosis Factor-alpha
Tissue
Oxidative Stress
Adiposity
Macrophages
Weights and Measures
Nutrition
Adipose Tissue
Theca Cells
Hyperandrogenism
Aptitude
Adipocytes

Keywords

  • Abdominal adiposity
  • Hyperandrogenism
  • Inflammation
  • Insulin resistance
  • Ovarian dysfunction
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Endocrinology
  • Molecular Biology
  • Organic Chemistry
  • Pharmacology

Cite this

Inflammation in Polycystic Ovary Syndrome : Underpinning of insulin resistance and ovarian dysfunction. / González, Frank.

In: Steroids, Vol. 77, No. 4, 10.03.2012, p. 300-305.

Research output: Contribution to journalArticle

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