Nutrient-Induced Inflammation in Polycystic Ovary Syndrome: Role in the Development of Metabolic Aberration and Ovarian Dysfunction

Frank González

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

A pathophysiology paradigm shift has emerged with the discovery that polycystic ovary syndrome (PCOS) is a proinflammatory state. Despite the dogma that the compensatory hyperinsulinemia of insulin resistance is the promoter of hyperandrogenism, physiological insulin infusion has no effect on androgen levels in PCOS. The dogma also does not explain the cause of hyperandrogenism and ovarian dysfunction in the 30 to 50% of women with PCOS who are of normal weight and lack insulin resistance. Inflammation is the underpinning of insulin resistance in obesity and type 2 diabetes, and may also be the cause of insulin resistance when present in PCOS. The origin of inflammation in PCOS has been ascribed to excess abdominal adiposity or frank obesity. However, nutrients such as glucose and saturated fat can incite inflammation from circulating mononuclear cells (MNC) of women with PCOS independent of excess adiposity and insulin resistance, and can also promote atherogenesis. Hyperandrogenism activates MNC in the fasting state to increase MNC sensitivity to nutrients, and is a potential mechanism for initiating inflammation in PCOS. However, chronic ovarian androgen suppression does not reduce inflammation in normal-weight women with PCOS. Direct exposure of ovarian theca cells to proinflammatory stimuli in vitro increases androgen production. These findings may be corroborated in vivo with anti-inflammatory therapy to normal-weight insulin-sensitive women with PCOS without abdominal adiposity to observe for amelioration of ovarian dysfunction.

Original languageEnglish
Pages (from-to)276-286
Number of pages11
JournalSeminars in Reproductive Medicine
Volume33
Issue number4
DOIs
StatePublished - Jul 3 2015

Fingerprint

Polycystic Ovary Syndrome
Inflammation
Food
Insulin Resistance
Hyperandrogenism
Adiposity
Androgens
Weights and Measures
Obesity
Insulin
Theca Cells
Hyperinsulinism
Type 2 Diabetes Mellitus
Fasting
Atherosclerosis
Anti-Inflammatory Agents
Fats
Glucose

Keywords

  • abdominal adiposity
  • hyperandrogenism
  • inflammation
  • insulin resistance
  • oxidative stress

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Physiology (medical)
  • Obstetrics and Gynecology
  • Reproductive Medicine

Cite this

Nutrient-Induced Inflammation in Polycystic Ovary Syndrome : Role in the Development of Metabolic Aberration and Ovarian Dysfunction. / González, Frank.

In: Seminars in Reproductive Medicine, Vol. 33, No. 4, 03.07.2015, p. 276-286.

Research output: Contribution to journalArticle

@article{c80df82465274320b933b108854ae8d3,
title = "Nutrient-Induced Inflammation in Polycystic Ovary Syndrome: Role in the Development of Metabolic Aberration and Ovarian Dysfunction",
abstract = "A pathophysiology paradigm shift has emerged with the discovery that polycystic ovary syndrome (PCOS) is a proinflammatory state. Despite the dogma that the compensatory hyperinsulinemia of insulin resistance is the promoter of hyperandrogenism, physiological insulin infusion has no effect on androgen levels in PCOS. The dogma also does not explain the cause of hyperandrogenism and ovarian dysfunction in the 30 to 50{\%} of women with PCOS who are of normal weight and lack insulin resistance. Inflammation is the underpinning of insulin resistance in obesity and type 2 diabetes, and may also be the cause of insulin resistance when present in PCOS. The origin of inflammation in PCOS has been ascribed to excess abdominal adiposity or frank obesity. However, nutrients such as glucose and saturated fat can incite inflammation from circulating mononuclear cells (MNC) of women with PCOS independent of excess adiposity and insulin resistance, and can also promote atherogenesis. Hyperandrogenism activates MNC in the fasting state to increase MNC sensitivity to nutrients, and is a potential mechanism for initiating inflammation in PCOS. However, chronic ovarian androgen suppression does not reduce inflammation in normal-weight women with PCOS. Direct exposure of ovarian theca cells to proinflammatory stimuli in vitro increases androgen production. These findings may be corroborated in vivo with anti-inflammatory therapy to normal-weight insulin-sensitive women with PCOS without abdominal adiposity to observe for amelioration of ovarian dysfunction.",
keywords = "abdominal adiposity, hyperandrogenism, inflammation, insulin resistance, oxidative stress",
author = "Frank Gonz{\'a}lez",
year = "2015",
month = "7",
day = "3",
doi = "10.1055/s-0035-1554918",
language = "English",
volume = "33",
pages = "276--286",
journal = "Seminars in Reproductive Medicine",
issn = "1526-8004",
publisher = "Thieme Medical Publishers",
number = "4",

}

TY - JOUR

T1 - Nutrient-Induced Inflammation in Polycystic Ovary Syndrome

T2 - Role in the Development of Metabolic Aberration and Ovarian Dysfunction

AU - González, Frank

PY - 2015/7/3

Y1 - 2015/7/3

N2 - A pathophysiology paradigm shift has emerged with the discovery that polycystic ovary syndrome (PCOS) is a proinflammatory state. Despite the dogma that the compensatory hyperinsulinemia of insulin resistance is the promoter of hyperandrogenism, physiological insulin infusion has no effect on androgen levels in PCOS. The dogma also does not explain the cause of hyperandrogenism and ovarian dysfunction in the 30 to 50% of women with PCOS who are of normal weight and lack insulin resistance. Inflammation is the underpinning of insulin resistance in obesity and type 2 diabetes, and may also be the cause of insulin resistance when present in PCOS. The origin of inflammation in PCOS has been ascribed to excess abdominal adiposity or frank obesity. However, nutrients such as glucose and saturated fat can incite inflammation from circulating mononuclear cells (MNC) of women with PCOS independent of excess adiposity and insulin resistance, and can also promote atherogenesis. Hyperandrogenism activates MNC in the fasting state to increase MNC sensitivity to nutrients, and is a potential mechanism for initiating inflammation in PCOS. However, chronic ovarian androgen suppression does not reduce inflammation in normal-weight women with PCOS. Direct exposure of ovarian theca cells to proinflammatory stimuli in vitro increases androgen production. These findings may be corroborated in vivo with anti-inflammatory therapy to normal-weight insulin-sensitive women with PCOS without abdominal adiposity to observe for amelioration of ovarian dysfunction.

AB - A pathophysiology paradigm shift has emerged with the discovery that polycystic ovary syndrome (PCOS) is a proinflammatory state. Despite the dogma that the compensatory hyperinsulinemia of insulin resistance is the promoter of hyperandrogenism, physiological insulin infusion has no effect on androgen levels in PCOS. The dogma also does not explain the cause of hyperandrogenism and ovarian dysfunction in the 30 to 50% of women with PCOS who are of normal weight and lack insulin resistance. Inflammation is the underpinning of insulin resistance in obesity and type 2 diabetes, and may also be the cause of insulin resistance when present in PCOS. The origin of inflammation in PCOS has been ascribed to excess abdominal adiposity or frank obesity. However, nutrients such as glucose and saturated fat can incite inflammation from circulating mononuclear cells (MNC) of women with PCOS independent of excess adiposity and insulin resistance, and can also promote atherogenesis. Hyperandrogenism activates MNC in the fasting state to increase MNC sensitivity to nutrients, and is a potential mechanism for initiating inflammation in PCOS. However, chronic ovarian androgen suppression does not reduce inflammation in normal-weight women with PCOS. Direct exposure of ovarian theca cells to proinflammatory stimuli in vitro increases androgen production. These findings may be corroborated in vivo with anti-inflammatory therapy to normal-weight insulin-sensitive women with PCOS without abdominal adiposity to observe for amelioration of ovarian dysfunction.

KW - abdominal adiposity

KW - hyperandrogenism

KW - inflammation

KW - insulin resistance

KW - oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=84934290630&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84934290630&partnerID=8YFLogxK

U2 - 10.1055/s-0035-1554918

DO - 10.1055/s-0035-1554918

M3 - Article

C2 - 26132932

AN - SCOPUS:84934290630

VL - 33

SP - 276

EP - 286

JO - Seminars in Reproductive Medicine

JF - Seminars in Reproductive Medicine

SN - 1526-8004

IS - 4

ER -