Document Detail


Genetic control of ATGL-mediated lipolysis modulates adipose triglyceride stores in leptin-deficient mice.
MedLine Citation:
PMID:  22383686     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Dissecting the genetics of complex traits such as obesity allows the identification of causal genes for disease. Here, we show that the BALB/c mouse strain carries genetic variants that confer resistance to obesity induced by leptin-deficiency or a high-fat diet (HFD). We set out to identify the physiological and genetic bases underlying this phenotype. When compared with C57BL6/J ob/ob mice (B6), BALB/c ob/ob mice exhibited decreased food intake, increased thermogenic capacity, and improved fat catabolism, each of which can potentially modify obesity. Interestingly, analysis of F1 ob/ob (progeny of B6 ob/+ × BALB/c ob+) mice revealed that obesity resistance in BALB/c ob/ob mice principally relied upon improved fat mobilization. This was mechanistically explained by increased adipose triglyceride lipase (ATGL) content in adipocytes, along with increased lipolysis and fatty acid oxidation. We conducted a genome-wide scan and defined a quantitative trait locus (QTL) on chromosome 2. BALB/c alleles on chromosome 2 not only associated with the obesity resistance phenotype but also supported increased ATGL content in adipose tissue. In summary, our study provides evidence that leptin-independent control of adipocyte lipolysis rates directly modifies the balance of macronutrient handling and is sufficient to regulate fat mass in the absence of alterations in food intake and energy expenditure.-Marcelin, G., S-M. Liu, X. Li, G. J. Schwartz, and S. Chua.
Authors:
Genevieve Marcelin; Shun-Mei Liu; Xiaosong Li; Gary J Schwartz; Streamson Chua
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-03-01
Journal Detail:
Title:  Journal of lipid research     Volume:  53     ISSN:  0022-2275     ISO Abbreviation:  J. Lipid Res.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-04-12     Completed Date:  2012-08-08     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0376606     Medline TA:  J Lipid Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  964-72     Citation Subset:  IM    
Affiliation:
Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / metabolism
Adipose Tissue / cytology,  metabolism*
Animals
Basal Metabolism / genetics
Chromosomes, Mammalian / genetics
Diabetes Mellitus / genetics,  prevention & control
Diet, High-Fat / adverse effects
Disease Resistance / genetics
Eating / genetics
Energy Metabolism / genetics
Fatty Acids / metabolism
Female
Intracellular Space / metabolism
Leptin / deficiency*
Lipase / metabolism*
Lipolysis / genetics*
Male
Mice
Obesity / genetics,  prevention & control
Oxidation-Reduction
Polymorphism, Single Nucleotide / genetics
Quantitative Trait Loci / genetics
Species Specificity
Triglycerides / metabolism*
Grant Support
ID/Acronym/Agency:
DK-020541/DK/NIDDK NIH HHS; DK-026687/DK/NIDDK NIH HHS; HD-058155/HD/NICHD NIH HHS; P01-DK-26687/DK/NIDDK NIH HHS; R01-DK-057621/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids; 0/Leptin; 0/Triglycerides; EC 3.1.1.1/desnutrin protein, mouse; EC 3.1.1.3/Lipase
Comments/Corrections

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


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