Document Detail


Inhibition of acyl-coenzyme A:cholesterol acyltransferase 2 (ACAT2) prevents dietary cholesterol-associated steatosis by enhancing hepatic triglyceride mobilization.
MedLine Citation:
PMID:  20231283     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acyl-CoA:cholesterol O-acyl transferase 2 (ACAT2) promotes cholesterol absorption by the intestine and the secretion of cholesteryl ester-enriched very low density lipoproteins by the liver. Paradoxically, mice lacking ACAT2 also exhibit mild hypertriglyceridemia. The present study addresses the unexpected role of ACAT2 in regulation of hepatic triglyceride (TG) metabolism. Mouse models of either complete genetic deficiency or pharmacological inhibition of ACAT2 were fed low fat diets containing various amounts of cholesterol to induce hepatic steatosis. Mice genetically lacking ACAT2 in both the intestine and the liver were dramatically protected against hepatic neutral lipid (TG and cholesteryl ester) accumulation, with the greatest differences occurring in situations where dietary cholesterol was elevated. Further studies demonstrated that liver-specific depletion of ACAT2 with antisense oligonucleotides prevents dietary cholesterol-associated hepatic steatosis both in an inbred mouse model of non-alcoholic fatty liver disease (SJL/J) and in a humanized hyperlipidemic mouse model (LDLr(-/-), apoB(100/100)). All mouse models of diminished ACAT2 function showed lowered hepatic triglyceride concentrations and higher plasma triglycerides secondary to increased hepatic secretion of TG into nascent very low density lipoproteins. This work demonstrates that inhibition of hepatic ACAT2 can prevent dietary cholesterol-driven hepatic steatosis in mice. These data provide the first evidence to suggest that ACAT2-specific inhibitors may hold unexpected therapeutic potential to treat both atherosclerosis and non-alcoholic fatty liver disease.
Authors:
Heather M Alger; J Mark Brown; Janet K Sawyer; Kathryn L Kelley; Ramesh Shah; Martha D Wilson; Mark C Willingham; Lawrence L Rudel
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-03-15
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  285     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-03     Completed Date:  2010-06-11     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  14267-74     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1040, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apolipoprotein B-100 / physiology
Blotting, Western
Cholesterol Esters / metabolism
Cholesterol, Dietary / administration & dosage
Fatty Liver / metabolism,  prevention & control*
Female
Hyperlipidemias / metabolism,  prevention & control*
Liver / metabolism*
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Oligonucleotides, Antisense / pharmacology
RNA, Messenger / genetics,  metabolism
Receptors, LDL / physiology
Reverse Transcriptase Polymerase Chain Reaction
Sterol O-Acyltransferase / antagonists & inhibitors,  physiology*
Triglycerides / metabolism*
Grant Support
ID/Acronym/Agency:
1K99-HL096166/HL/NHLBI NIH HHS; HL-49373/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Apolipoprotein B-100; 0/Cholesterol Esters; 0/Cholesterol, Dietary; 0/Oligonucleotides, Antisense; 0/RNA, Messenger; 0/Receptors, LDL; 0/Triglycerides; EC 2.3.1.26/Sterol O-Acyltransferase; EC 2.3.1.26/sterol O-acyltransferase 2
Comments/Corrections

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