Document Detail


Regulation of fatty acid and cholesterol synthesis: co-operation or competition?
MedLine Citation:
PMID:  14559068     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fatty acids and sterols originally evolved symbiotically as structural components of cell membranes. In some respects, control of their biosynthetic pathways reflects their mutual interdependence in defining changes in the physicochemical properties of the membranes in response to the changing internal and external cellular environments. In some tissues of higher animals, however, cholesterol and fatty acids have multifunctional roles. In particular, the liver synthesizes these lipids for export as multimolecular complexes in the form of micellar bile components and lipoproteins. Intrahepatic fatty acid and cholesterol synthesis is dependent upon the balance between hepatic output of these complexes and dietary input of fat and cholesterol. Thus physiological control of these synthetic processes is often co-ordinated at both the transcriptional and post-translational levels. On the other hand, changes in flux through major metabolic pathways, particularly during physiological transitions and as a result of genetic manipulation, affects substrate availability for these pathways. Under these circumstances, regulation reflects a compensatory response to ensure that flux through the lipid pathways remains unchanged. These regulatory changes can best be interpreted in terms of a Metabolic Control Analysis approach. In summary, flux through the fatty acid and cholesterol pathways reflects (a) cellular demand for these lipids, (b) a variable availability of substrates, (c) a combination of (a) and (b).
Authors:
Geoffrey F Gibbons
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Progress in lipid research     Volume:  42     ISSN:  0163-7827     ISO Abbreviation:  Prog. Lipid Res.     Publication Date:  2003 Nov 
Date Detail:
Created Date:  2003-10-15     Completed Date:  2004-02-10     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  7900832     Medline TA:  Prog Lipid Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  479-97     Citation Subset:  IM    
Affiliation:
Metabolic Research Laboratory, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Nuffield Department of Clinical Medicine, University of Oxford, Churchill Hospital, Old Road, Headington, OX3 7LJ, Oxford, UK.
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MeSH Terms
Descriptor/Qualifier:
Arteriosclerosis / metabolism
CCAAT-Enhancer-Binding Proteins / metabolism
Cell Membrane / metabolism*
Cholesterol / biosynthesis*
Cholesterol, Dietary / metabolism
DNA-Binding Proteins / metabolism
Fatty Acids / biosynthesis*
Homeostasis
Humans
Hydroxymethylglutaryl CoA Reductases / metabolism
Lipid Metabolism
Liver / metabolism*
Sterol Regulatory Element Binding Protein 1
Transcription Factors*
Chemical
Reg. No./Substance:
0/CCAAT-Enhancer-Binding Proteins; 0/Cholesterol, Dietary; 0/DNA-Binding Proteins; 0/Fatty Acids; 0/SREBF1 protein, human; 0/Sterol Regulatory Element Binding Protein 1; 0/Transcription Factors; 57-88-5/Cholesterol; EC 1.1.1.-/Hydroxymethylglutaryl CoA Reductases

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


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