Document Detail


The determinants of insulin sensitivity, β-cell function, and glucose tolerance are different in patients with polycystic ovary syndrome than in women who do not have hyperandrogenism.
MedLine Citation:
PMID:  20097337     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To evaluate the pathogenetic mechanisms underlying abnormal glucose tolerance in polycystic ovary syndrome (PCOS).
DESIGN: Case-control study.
SETTING: Academic hospital.
PATIENT(S): One hundred twelve patients with PCOS and 86 nonhyperandrogenic control women of similar age and body mass index (BMI).
INTERVENTION(S): An oral glucose tolerance test (OGTT) served to explore glucose tolerance and to calculate insulin sensitivity, insulin secretion, and insulin disposition indexes.
MAIN OUTCOME MEASURE(S): Frequency of abnormal glucose tolerance, indexes of insulin sensitivity, secretion and disposition, and markers of inflammation, androgen excess, and iron stores.
RESULT(S): Obesity and age, but not PCOS, were associated with an increased frequency of abnormal glucose tolerance and diabetes. An imbalance between insulin resistance and secretion--translated into decreased insulin disposition index--predicted abnormal glucose tolerance in patients with PCOS and controls, yet these women differed in the factors associated with decreased insulin disposition. In patients with PCOS, hyperandrogenism, chronic inflammation, and family history of diabetes contributed to insulin resistance as the main pathogenetic mechanism. In nonhyperandrogenic women, familial aggregation of defective insulin secretion, adiposity, and increased body iron stores explained most of the decrease in insulin disposition.
CONCLUSION(S): In addition to a major influence of obesity and age, the mechanisms underlying abnormal glucose tolerance are different in patients with PCOS compared with women who do not have hyperandrogenism.
Authors:
Manuel Luque-Ramírez; Macarena Alpañés; Héctor F Escobar-Morreale
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-25
Journal Detail:
Title:  Fertility and sterility     Volume:  94     ISSN:  1556-5653     ISO Abbreviation:  Fertil. Steril.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-27     Completed Date:  2010-12-08     Revised Date:  2012-04-09    
Medline Journal Info:
Nlm Unique ID:  0372772     Medline TA:  Fertil Steril     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2214-21     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
Affiliation:
Department of Endocrinology, Hospital Universitario Ramón y Cajal and Universidad de Alcalá, Madrid, Madrid, Spain.
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MeSH Terms
Descriptor/Qualifier:
Adiponectin / blood,  metabolism
Biological Markers / analysis*,  blood,  metabolism
Blood Glucose / metabolism*
Case-Control Studies
Female
Ferritins / blood,  metabolism
Glucose Intolerance / blood,  complications,  diagnosis,  metabolism
Humans
Hyperandrogenism / blood,  metabolism,  physiopathology
Inflammation Mediators / blood,  metabolism
Insulin / secretion
Insulin Resistance / physiology*
Insulin-Secreting Cells / physiology*
Odds Ratio
Polycystic Ovary Syndrome / blood,  diagnosis,  metabolism*,  physiopathology*
Chemical
Reg. No./Substance:
0/ADIPOQ protein, human; 0/Adiponectin; 0/Biological Markers; 0/Blood Glucose; 0/Inflammation Mediators; 0/Insulin; 9007-73-2/Ferritins

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