Document Detail


The Moo1 obesity quantitative trait locus in BTBR T+ Itpr3tf/J mice increases food intake.
MedLine Citation:
PMID:  23341217     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The rising prevalence of obesity is one of the greatest health challenges facing the world today. Discovery of genetic factors affecting obesity risk will provide important insight to its etiology that could suggest new therapeutic approaches. We have previously identified the Modifier of obese 1 (Moo1) quantitative trait locus (QTL) in a cross between leptin-deficient BTBR T(+) Itpr3(tf)/J (BTBR) and C57BL/6J (B6) mice. Understanding the mechanism by which this locus acts will aid in the identification of candidate genes. Here we refined the location of this QTL and sought to determine the mechanism by which Moo1 affects body weight. We found that the effects of Moo1 also alter high fat diet-induced obesity in mice having functional leptin. In detailed metabolic analyses we determined that this locus acts by increasing food intake in BTBR mice, without affecting energy expenditure. The increased food intake associated with BTBR alleles at Moo1 likely results from increased meal size. Finally, we show that the increased adiposity resulting from Moo1 is sufficient to affect glucose tolerance. These studies show that the Moo1 obesity QTL affects food intake in a manner independent of leptin and indicate that modulation of the underlying pathway may not only ameliorate obesity but also its clinical consequences.
Authors:
Subashini Karunakaran; Akiff Manji; Chenhua Serena Yan; Zi-Jun John Wu; Susanne Michelle Clee
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-1-22
Journal Detail:
Title:  Physiological genomics     Volume:  -     ISSN:  1531-2267     ISO Abbreviation:  Physiol. Genomics     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-1-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9815683     Medline TA:  Physiol Genomics     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
University of British Columbia.
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