Document Detail


The development of a metabolic disease phenotype in CTP:phosphoethanolamine cytidylyltransferase-deficient mice.
MedLine Citation:
PMID:  19625253     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Phosphatidylethanolamine (PE) is an important inner membrane phospholipid mostly synthesized de novo via the PE-Kennedy pathway and by the decarboxylation of phosphatidylserine. CTP:phosphoethanolamine cytidylyltransferase (Pcyt2) catalyzes the formation of CDP-ethanolamine, which is often the rate regulatory step in the PE-Kennedy pathway. In the current investigation, we show that the reduced CDP-ethanolamine formation in Pcyt2(+/-) mice limits the rate of PE synthesis and increases the availability of diacylglycerol. This results in the increased formation of triglycerides, which is facilitated by stimulated de novo fatty acid synthesis and increased uptake of pre-existing fatty acids. Pcyt2(+/-) mice progressively accumulate more diacylglycerol and triglycerides with age and have modified fatty acid composition, predominantly in PE and triglycerides. Pcyt2(+/-) additionally have an inherent blockage in fatty acid utilization as energy substrate and develop impaired tolerance to glucose and insulin at an older age. Accordingly, gene expression analyses demonstrated the up-regulation of the main lipogenic genes and down-regulation of mitochondrial fatty acid beta-oxidation genes. These data demonstrate for the first time that to preserve membrane PE phospholipids, Pcyt2 deficiency generates compensatory changes in triglyceride and energy substrate metabolism, resulting in a progressive development of liver steatosis, hypertriglyceridemia, obesity, and insulin resistance, the main features of the metabolic syndrome.
Authors:
Morgan D Fullerton; Fatima Hakimuddin; Arend Bonen; Marica Bakovic
Related Documents :
5810083 - N-acylphosphatidylethanolamine, a phospholipid that is rapidly metabolized during the a...
8973583 - Origin of hepatic very-low-density lipoprotein triacylglycerol: the contribution of cel...
7932163 - Serotonin inhibits gastric acid secretion through a 5-hydroxytryptamine1-like receptor ...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-07-22
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  284     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-09-14     Completed Date:  2009-10-19     Revised Date:  2010-09-21    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  25704-13     Citation Subset:  IM    
Affiliation:
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cytidine Diphosphate / analogs & derivatives*,  genetics,  metabolism
Diglycerides / genetics,  metabolism
Ethanolamines / metabolism*
Fatty Liver / enzymology,  genetics
Female
Gene Expression Regulation / genetics
Hypertriglyceridemia / enzymology,  genetics
Insulin Resistance / genetics
Lipid Metabolism, Inborn Errors / enzymology*,  genetics
Male
Metabolic Syndrome X / enzymology,  genetics
Mice
Mice, Knockout
Phosphatidylethanolamines / biosynthesis*,  genetics
Phosphatidylserines / genetics,  metabolism
RNA Nucleotidyltransferases*
Triglycerides / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Diglycerides; 0/Ethanolamines; 0/Phosphatidylethanolamines; 0/Phosphatidylserines; 0/Triglycerides; 3036-18-8/CDP ethanolamine; 39382-08-6/phosphatidylethanolamine; 63-38-7/Cytidine Diphosphate; EC 2.7.7.-/RNA Nucleotidyltransferases; EC 2.7.7.14/Ethanolamine-phosphate cytidylyltransferase

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


Previous Document:  SCHEMA recombination of a fungal cellulase uncovers a single mutation that contributes markedly to s...
Next Document:  Targeted inactivation of a developmentally regulated neural plectin isoform (plectin 1c) in mice lea...