Document Detail


Adipose triglyceride lipase is implicated in fuel- and non-fuel-stimulated insulin secretion.
MedLine Citation:
PMID:  19389712     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Reduced lipolysis in hormone-sensitive lipase-deficient mice is associated with impaired glucose-stimulated insulin secretion (GSIS), suggesting that endogenous beta-cell lipid stores provide signaling molecules for insulin release. Measurements of lipolysis and triglyceride (TG) lipase activity in islets from HSL(-/-) mice indicated the presence of other TG lipase(s) in the beta-cell. Using real time-quantitative PCR, adipose triglyceride lipase (ATGL) was found to be the most abundant TG lipase in rat islets and INS832/13 cells. To assess its role in insulin secretion, ATGL expression was decreased in INS832/13 cells (ATGL-knockdown (KD)) by small hairpin RNA. ATGL-KD increased the esterification of free fatty acid (FFA) into TG. ATGL-KD cells showed decreased glucose- or Gln + Leu-induced insulin release, as well as reduced response to KCl or palmitate at high, but not low, glucose. The K(ATP)-independent/amplification pathway of GSIS was considerably reduced in ATGL-KD cells. ATGL(-/-) mice were hypoinsulinemic and hypoglycemic and showed decreased plasma TG and FFAs. A hyperglycemic clamp revealed increased insulin sensitivity and decreased GSIS and arginine-induced insulin secretion in ATGL(-/-) mice. Accordingly, isolated islets from ATGL(-/-) mice showed reduced insulin secretion in response to glucose, glucose + palmitate, and KCl. Islet TG content and FFA esterification into TG were increased by 2-fold in ATGL(-/-) islets, but glucose usage and oxidation were unaltered. The results demonstrate the importance of ATGL and intracellular lipid signaling for fuel- and non-fuel-induced insulin secretion.
Authors:
Marie-Line Peyot; Claudiane Guay; Martin G Latour; Julien Lamontagne; Roxane Lussier; Marco Pineda; Neil B Ruderman; Guenter Haemmerle; Rudolf Zechner; Erik Joly; S R Murthy Madiraju; Vincent Poitout; Marc Prentki
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-04-22
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  284     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-06-15     Completed Date:  2009-10-20     Revised Date:  2010-09-24    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  16848-59     Citation Subset:  IM    
Affiliation:
Molecular Nutrition Unit and Montreal Diabetes Research Center, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montreal, Quebec H1W4A4, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Base Sequence
Carboxylic Ester Hydrolases / deficiency,  genetics,  metabolism*
Cell Line
Fasting / metabolism
Fatty Acids, Nonesterified / metabolism
Glucose / pharmacology
Glucose Clamp Technique
Insulin / secretion*
Islets of Langerhans / drug effects,  metabolism,  secretion
Lipase / antagonists & inhibitors,  genetics,  metabolism
Lipolysis
Male
Mice
Mice, Knockout
RNA, Small Interfering / genetics
Rats
Signal Transduction
Triglycerides / metabolism
Chemical
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 0/RNA, Small Interfering; 0/Triglycerides; 11061-68-0/Insulin; 50-99-7/Glucose; EC 3.1.1.-/Carboxylic Ester Hydrolases; 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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