Document Detail


Interaction of genetic and environmental programming of the leptin system and of obesity disposition.
MedLine Citation:
PMID:  11015606     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Possible adverse interactions between an usually inconspicuous genetic trait and early environmental factors favoring the development of obesity were investigated in rats heterozygous for the leptin receptor defect "fatty" (fa). Pups were exposed to early postnatal overfeeding by reducing litter size from normally 10-12 to only 4. Rearing +/+ and +/fa pups from day 3 to 21 in small litters increased fat-free dry mass and body fat, but only in the latter did a significant interaction with genotype occur. Pronounced differences in the responsiveness of +/+ and +/fa pups to "prophylactic" leptin treatment (from day 1 to 21) were observed, with +/fa females from small litters being nearly as fat and unresponsive as previously reported for normally reared fa/fa pups. Clear heterozygous differences in total hypothalamic leptin binding, but no litter size effect, paralleling the differences in leptin responsiveness, were observed. By early postnatal overfeeding an usually inconspicuous genetic trait may thus become etiologic for the development of obesity via physiological changes other than the decreased leptin binding characterizing the genetic defect.
Authors:
I Schmidt; C Schoelch; T Ziska; D Schneider; E Simon; A Plagemann
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2000-08-09
Journal Detail:
Title:  Physiological genomics     Volume:  3     ISSN:  1531-2267     ISO Abbreviation:  Physiol. Genomics     Publication Date:  2000 Aug 
Date Detail:
Created Date:  2000-10-12     Completed Date:  2000-10-27     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9815683     Medline TA:  Physiol Genomics     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  113-20     Citation Subset:  IM    
Affiliation:
Max-Planck-Institut für physiologische und klinische Forschung, W. G. Kerckhoff-Institut, D-61231 Bad Nauheim, Germany. I.Schmidt@kerckhoff.mpg.de
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / drug effects,  growth & development
Analysis of Variance
Animals
Body Composition / drug effects
Body Weight / drug effects
Carrier Proteins / metabolism*
Environment*
Female
Gene Deletion
Genetic Predisposition to Disease*
Heterozygote
Homozygote
Hypothalamus / metabolism
Least-Squares Analysis
Leptin / blood,  metabolism*,  pharmacology
Litter Size
Male
Obesity / blood,  genetics*
Rats
Rats, Mutant Strains
Rats, Zucker
Receptors, Cell Surface*
Receptors, Leptin
Software
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Leptin; 0/Receptors, Cell Surface; 0/Receptors, Leptin

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


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