Document Detail


Effect of food restriction and leptin supplementation on fetal programming in mice.
MedLine Citation:
PMID:  22778222     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Metabolic disease is a significant global health and economic problem. In a phenomenon referred to as fetal programming, offspring of underweight or overweight mothers have an increased incidence of adulthood obesity and metabolic disease. Undernourished individuals have decreased levels of leptin, a regulator of energy balance, whereas obese people develop hyperleptinemia and leptin resistance. We hypothesize that alterations in circulating leptin during pregnancy contribute to programming events caused by maternal nutritional status. To test this hypothesis, pregnant mice were randomly placed in one of three treatment groups: ad libitum feed plus saline injection (control, n = 5), 50% food restriction plus saline injection (restricted, n = 4), or 50% food restriction plus 1 mg/kg · d leptin injection (restricted, leptin treated, n = 4). Mice were treated from 1.5 to 11.5 d after conception and then returned to ad libitum feeding until weaning. At 19 wk after weaning, offspring were placed on a 45% fat diet and then followed up until 26 wk after weaning, at which time they were killed, and samples were collected for further analysis. Our results demonstrate that males are more negatively impacted by high-fat diet than females, regardless of maternal treatment. We provide evidence that differential response to leptin may mediate the sexual dimorphism observed in fetal programming in which male offspring are more affected by maternal undernutrition and female offspring by maternal overnutrition. We show that female offspring born to food-restricted, leptin-supplemented mothers are obese and insulin resistant. This may mimic fetal programming events seen in offspring of overweight women.
Authors:
Kathleen A Pennington; Jennifer L Harper; Ashley N Sigafoos; Lindsey M Beffa; Stephanie M Carleton; Charlotte L Phillips; Laura C Schulz
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-07-09
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-08-24     Completed Date:  2012-10-29     Revised Date:  2013-09-03    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4556-67     Citation Subset:  AIM; IM    
Affiliation:
Division of Reproductive and Perinatal Research, Department of Obstetrics, Gynecology, and Women's Health, University of Missouri, 1 Hospital Drive, Columbia, Missouri 65212, USA. penningtonka@health.missouri.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Female
Fetal Development / drug effects*
Food Deprivation / physiology*
Leptin / pharmacology*
Mice
Pregnancy
Grant Support
ID/Acronym/Agency:
HD055231/HD/NICHD NIH HHS; R00 HD055231/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Leptin
Comments/Corrections

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


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