Document Detail


Reduction in cholesterol synthesis in response to serum starvation in lymphoblasts of a patient with Barth syndrome.
MedLine Citation:
PMID:  20651830     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Barth syndrome is a rare X-linked disease in which mild hypocholesterolemia is observed in some patients. We investigated cholesterol biosynthesis in lymphoblasts from a normal and age-matched Barth syndrome patient. Control and Barth syndrome (DeltaTAZ1) lymphoblasts were incubated in the presence or absence of serum to induce cholesterol synthesis and hydroxymethylglutaryl-coenzyme A reductase activity and expression, and cholesterol biosynthesis from radioactive precursors was determined. Cholesterol biosynthesis from [2-14C]pyruvate was stimulated 2-fold in control cells, but was unchanged in DeltaTAZ1 lymphoblasts, and from [1-14C]acetate was stimulated 77% in control but only 26% in DeltaTAZ1 lymphoblasts upon serum removal, indicating a lower ability of DeltaTAZ1 cells to upregulate cholesterol biosynthesis. The reason was an inability to increase hydroxymethylglutaryl-coenzyme A reductase activity, which was already near maximum in DeltaTAZ1 lymphoblasts, in response to serum removal, compared with control cells. The reduced ability to increase hydroxymethylglutaryl-coenzyme A reductase enzyme activity in DeltaTAZ1 lymphoblasts was due to a decrease in hydroxymethylglutaryl-coenzyme A reductase messenger RNA. Although total cholesterol levels are similar under standard culture conditions, DeltaTAZ1 lymphoblasts have a diminished capacity to respond to increased demand for cholesterol biosynthesis because of an already elevated level of synthesis under standard culture conditions.
Authors:
Kristin D Hauff; Grant M Hatch
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biochemistry and cell biology = Biochimie et biologie cellulaire     Volume:  88     ISSN:  1208-6002     ISO Abbreviation:  Biochem. Cell Biol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-23     Completed Date:  2010-12-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8606068     Medline TA:  Biochem Cell Biol     Country:  Canada    
Other Details:
Languages:  eng     Pagination:  595-602     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Therapeutics, Center for Research and Treatment of Atherosclerosis, Center on Aging, Faculty of Medicine, University of Manitoba, Winnipeg, MB, Canada.
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MeSH Terms
Descriptor/Qualifier:
ATP-Binding Cassette Transporters / genetics,  metabolism
Acetic Acid / pharmacokinetics
Barth Syndrome / genetics,  metabolism,  pathology*
Carbon Radioisotopes / pharmacokinetics
Cells, Cultured
Cholesterol / biosynthesis*
Culture Media, Serum-Free / pharmacology*
Gene Deletion
Gene Expression Regulation / drug effects
Humans
Hydroxymethylglutaryl CoA Reductases / genetics,  metabolism
Lymphocytes / drug effects*,  metabolism,  pathology*
Pyruvic Acid / pharmacokinetics
Receptors, LDL / genetics,  metabolism
Starvation / metabolism
Transcription Factors / genetics
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/ATP binding cassette transporter 1; 0/ATP-Binding Cassette Transporters; 0/Carbon Radioisotopes; 0/Culture Media, Serum-Free; 0/Receptors, LDL; 0/TAZ protein, human; 0/Transcription Factors; 127-17-3/Pyruvic Acid; 57-88-5/Cholesterol; 64-19-7/Acetic Acid; EC 1.1.1.-/Hydroxymethylglutaryl CoA Reductases

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


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