Document Detail


Evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease.
MedLine Citation:
PMID:  16142397     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of abnormal liver dysfunction, and its prevalence has markedly increased; however, the mechanisms involved in the pathogenesis of NAFLD have not been thoroughly investigated in humans. In this study, we evaluated the expression of fatty acid metabolism-related genes in NAFLD. Real-time RT-PCR was performed using liver biopsy samples from 12 NAFLD patients. The target genes studied were: acetyl-CoA carboxylase (ACC) 1, ACC2, and fatty acid synthase (FAS) for the evaluation of de novo fatty acid synthesis; carnitine palmitoyltransferase 1a (CPT1a), long-chain acyl-CoA dehydrogenase (LCAD), and long-chain L-3-hydroxyacyl-coenzyme A dehydrogenase alpha (HADHalpha) for beta-oxidation in the mitochondria; peroxisome proliferator-activated receptor- (PPAR-) alpha and cytochrome P450 2E1 (CYP2E1) for oxidation in peroxisomes and microsomes (endoplasmic reticulum) respectively; and diacylglycerol O-acyltransferase 1 (DGAT1), PPAR-gamma, and hormone sensitive lipase (HSL) for triglyceride synthesis and catalysis. In NAFLD, expression of ACC1 and ACC2, but not FAS was increased, indicating that de novo fatty acid synthesis is enhanced in NAFLD. In contrast, expression of CTP1a, a rate-limiting enzyme, was remarkably decreased, indicating that beta-oxidation in the mitochondria was decreased, although the expression of LCAD and HADHalpha was increased. Expression of PPAR-alpha was increased, whereas that of CYP2E1 was reduced. The expression of DGAT1, PPAR-gamma, and HSL was enhanced. These data suggest that in NAFLD, increased de novo synthesis and decreased beta-oxidation in the mitochondria lead to accumulation of fatty acids in hepatocytes, although the extent of oxidation in peroxisomes and microsomes remains unclear.
Authors:
Makoto Nakamuta; Motoyuki Kohjima; Shusuke Morizono; Kazuhiro Kotoh; Tsuyoshi Yoshimoto; Izuru Miyagi; Munechika Enjoji
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  International journal of molecular medicine     Volume:  16     ISSN:  1107-3756     ISO Abbreviation:  Int. J. Mol. Med.     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2005-09-05     Completed Date:  2005-12-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9810955     Medline TA:  Int J Mol Med     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  631-5     Citation Subset:  IM    
Affiliation:
Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. nakamuta@intmed3.med.kyushu-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Biopsy
Fatty Acids / metabolism*
Fatty Liver / genetics*,  metabolism,  pathology
Gene Expression Profiling*
Humans
Lipids / biosynthesis
Liver / metabolism,  pathology
Mitochondria / metabolism
Oxidation-Reduction
RNA / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Chemical
Reg. No./Substance:
0/Fatty Acids; 0/Lipids; 63231-63-0/RNA

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