Document Detail


Large litter rearing enhances leptin sensitivity and protects selectively bred diet-induced obese rats from becoming obese.
MedLine Citation:
PMID:  20668022     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Because rearing rats in large litters (LLs) protects them from becoming obese, we postulated that LL rearing would protect rats selectively bred to develop diet-induced obesity (DIO) from becoming obese by overcoming their inborn central leptin resistance. Male and female DIO rats were raised in normal litters (NLs; 10 pups/dam) or LLs (16 pups/dam) and assessed for anatomical, biochemical, and functional aspects of leptin sensitivity at various ages when fed low-fat chow or a 31% fat high-energy (HE) diet. LL rearing reduced plasma leptin levels by postnatal day 2 (P2) and body weight gain by P8. At P16, LL DIO neonates had increased arcuate nucleus (ARC) binding of leptin to its extracellular receptors and at P28 an associated increase of their agouti-related peptide and alpha-MSH axonal projections to the paraventricular nucleus. Reduced body weight persisted and was associated with increased ARC leptin receptor binding and sensitivity to the anorectic effects of leptin, reduced adiposity, and enhanced insulin sensitivity in LL DIO rats fed chow until 10 wk of age. The enhanced ARC leptin receptor binding and reduced adiposity of LL DIO rats persisted after an additional 5 wk on the HE diet. Female LL DIO rats had similar reductions in weight gain on both chow and HE diet vs. normal litter DIO rats. We postulate that LL rearing enhances DIO leptin sensitivity by lowering plasma leptin levels and thereby increasing leptin receptor availability and that this both enhances the ARC-paraventricular nucleus pathway development and protects them from becoming obese.
Authors:
Christa M Patterson; Sebastien G Bouret; Sunny Park; Boman G Irani; Ambrose A Dunn-Meynell; Barry E Levin
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-07-28
Journal Detail:
Title:  Endocrinology     Volume:  151     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-25     Completed Date:  2010-10-04     Revised Date:  2011-09-13    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4270-9     Citation Subset:  AIM; IM    
Affiliation:
Division of Metabolism, Endocrinology, and Diabetes, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA.
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MeSH Terms
Descriptor/Qualifier:
Adiposity / physiology
Agouti-Related Protein / metabolism
Animals
Animals, Newborn
Arcuate Nucleus / metabolism
Body Weight / physiology
Breeding
Diet*
Eating / physiology
Female
Gestational Age
Immunohistochemistry
Lactation / physiology
Leptin / blood*,  metabolism
Litter Size / physiology*
Male
Obesity / blood,  etiology,  physiopathology*
Paraventricular Hypothalamic Nucleus / metabolism
Protein Binding
Rats
Receptors, Leptin / metabolism
Time Factors
Weaning
Weight Gain / physiology
alpha-MSH / metabolism
Grant Support
ID/Acronym/Agency:
F31-NS-050903/NS/NINDS NIH HHS; NIDDK R01-30066//PHS HHS
Chemical
Reg. No./Substance:
0/AGRP protein, rat; 0/Agouti-Related Protein; 0/Leptin; 0/Receptors, Leptin; 581-05-5/alpha-MSH
Comments/Corrections

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