Document Detail


Genetic deficiency for proprotein convertase subtilisin/kexin type 2 in mice is associated with decreased adiposity and protection from dietary fat-induced body weight gain.
MedLine Citation:
PMID:  20498660     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
BACKGROUND: Proprotein convertase subtilisin/xexin type 2 (PCSK2) is an endoproteinase responsible for proteolytic activation of a number of precursors to active neuropeptides and peptide hormones, known to influence glucose homeostasis, food intake and ultimately body mass. In this study, we examined the consequences of PCSK2 deficiency on these phenotypic traits.
STUDY DESIGN: Weight gain with age under diets of different fat contents was monitored. White adipose tissue (WAT) and muscle masses were evaluated. Plasma levels of triglycerides, leptin, ghrelin, insulin and proglucagon-derived peptides were measured as well as leptin and acetyl coenzyme-α carboxylase (ACCα) mRNA levels in adipose tissue.
RESULTS: Compared with their Pcsk2 (+/+) littermates, Pcsk2 (-/-) mice weighed significantly less as weanlings and as adults. As adults, they carried noticeably less fat mass, with similar lean muscle mass: their plasma leptin level and adipose tissue leptin mRNA level were accordingly lower. PCSK2 deficiency did not affect food intake or the level of the orexigenic hormone ghrelin. However, PCSK2 deficiency resulted in decreased plasma triglycerides and reduced ACCα mRNA levels in WAT. Interestingly, unlike their Pcsk2 (+/+) littermates, Pcsk2 (-/-) were resistant to enhanced body weight gain when fed a high-fat diet. Consistent with a role of PCSK2 in body mass gain, diet-induced or genetically obese mice were found to contain significantly higher levels of PCSK2 mRNA in their brain and stomach than their lean counterparts.
CONCLUSION: Collectively, these results suggest that PCSK2 contributes to increase in body mass through the various regulatory peptides generated through its action. It represents a potential target in the prevention and treatment of obesity.
Authors:
Y Anini; J Mayne; J Gagnon; J Sherbafi; A Chen; N Kaefer; M Chrétien; M Mbikay
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-05-25
Journal Detail:
Title:  International journal of obesity (2005)     Volume:  34     ISSN:  1476-5497     ISO Abbreviation:  Int J Obes (Lond)     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-15     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101256108     Medline TA:  Int J Obes (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  1599-607     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada. younes.anini@dal.ca
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research

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


Previous Document:  A unique genetic defect on chromosome 3 is responsible for juvenile obesity in the Berlin Fat Mouse.
Next Document:  Trends in overweight and misperceived overweight in Spain from 1987 to 2007.