Document Detail


Developmental programming: insulin sensitizer treatment improves reproductive function in prenatal testosterone-treated female sheep.
MedLine Citation:
PMID:  20555028     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Prenatal testosterone (T) excess causes reproductive and metabolic disruptions including insulin resistance, attributes of women with polycystic ovary syndrome. This study tested the hypothesis that insulin resistance contributes toward severity of reproductive disruptions in prenatally T-treated females. Pregnant sheep were injected im with 100 mg of T-propionate semiweekly from d 30-90 of gestation. Immediately after the first breeding season, a subset of controls and prenatal T-treated (TR) sheep were administered an insulin sensitizer (rosiglitazone; 8 mg/d) orally for 8 months. Untreated control and prenatal T-treated females (T group) were studied in parallel. Biochemical analyses revealed rosiglitazone to be safe for use in sheep. Glucose tolerance tests performed before and after the insulin sensitizer treatment found that insulin sensitizer decreased cumulative insulin, cumulative insulin/glucose ratio, and insulin area under the curve by about 50% and increased the insulin sensitivity index by about 70% in the TR compared with the T group. Twenty percent of TR females showed a reduced number of cycles in the second relative to first breeding season as opposed to 80% of T group females showing such deterioration. Insulin sensitizer treatment also decreased the number of aberrant cycles (>/=18 d) during the second breeding season in the TR group relative to the first as opposed to the T group females showing an increase in the second breeding season relative to the first. These findings provide evidence that insulin sensitizer treatment prevents further deterioration of the reproductive axis in prenatal T-treated sheep, a finding of translational relevance to women with polycystic ovary syndrome.
Authors:
Almudena Veiga-Lopez; James S Lee; Vasantha Padmanabhan
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2010-06-16
Journal Detail:
Title:  Endocrinology     Volume:  151     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-27     Completed Date:  2010-09-08     Revised Date:  2011-08-03    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4007-17     Citation Subset:  AIM; IM    
Affiliation:
Department of Pediatrics and Reproductive Sciences Program, University of Michigan, Ann Arbor, Michigan 48109-0404, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Drug Evaluation, Preclinical
Estrous Cycle / blood,  drug effects,  metabolism
Female
Fetal Development / drug effects*
Hypoglycemic Agents / pharmacology
Insulin / metabolism*,  pharmacology
Insulin Resistance / physiology
Liver / metabolism,  physiopathology
Polycystic Ovary Syndrome / chemically induced,  drug therapy,  metabolism,  pathology
Pregnancy
Prenatal Exposure Delayed Effects / chemically induced*,  drug therapy*,  metabolism,  physiopathology
Reproduction / drug effects*,  physiology
Sheep
Testosterone / adverse effects*,  pharmacology
Thiazolidinediones / pharmacology,  therapeutic use*
Grant Support
ID/Acronym/Agency:
P01 HD44232/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Hypoglycemic Agents; 0/Thiazolidinediones; 11061-68-0/Insulin; 122320-73-4/rosiglitazone; 58-22-0/Testosterone
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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