Document Detail


A novel potent synthetic steroidal liver X receptor agonist lowers plasma cholesterol and triglycerides and reduces atherosclerosis in LDLR(-/-) mice.
MedLine Citation:
PMID:  21232031     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: Potent synthetic nonsteroidal liver X receptor (LXR) agonists like T0901317 induce triglyceridaemia and fatty liver, effects not observed with some natural and synthetic steroidal, relatively weak agonists of LXR. To determine if potency is responsible for the lack of side effects with some steroidal agonists, we investigated the in vivo effects of a novel steroidal LXR agonist, ATI-111, that is more potent than T0901317.
EXPERIMENTAL APPROACH: Eight week old male LDLR(-/-) mice fed an atherogenic diet were orally treated with vehicle or ATI-111 at 3 and 5 mg·kg(-1) ·day(-1) for 8 weeks, and effects on plasma and liver lipid levels, expression of genes involved in lipid metabolism and on atherogenesis were analysed.
KEY RESULTS: ATI-111 increased the expression of genes involved in lipid transport, such as ABCA1, ABCG1 and ABCG5/G8, in intestine and macrophages; decreased ABCG1, apoE; and slightly increased ABCA1 and ABCG5/G8 expression in liver. ATI-111 markedly increased sterol regulatory element-binding protein (SREBP)-1c mRNA in some tissues, whereas acetyl-coenzyme A carboxylase and fatty acid synthase expression was unaffected or only slightly increased in intestine and liver. ATI-111 inhibited the conversion of SREBP-1c precursor form to its active form. Compared with vehicle-treated mice, the levels of hepatic lipids and liver-secreted nascent lipoproteins were not altered, while a significant decrease in plasma cholesterol and triglyceride levels was observed in ATI-111-treated mice. ATI-111 significantly inhibited atherogenesis in three separate vascular sites.
CONCLUSIONS AND IMPLICATIONS: ATI-111 is a promising candidate for further development as a treatment of certain vascular diseases as it lacks the significant side effects associated with nonsteroidal LXR agonists, the induction of fatty liver and hypertriglyceridaemia.
Authors:
Dacheng Peng; Richard A Hiipakka; Jing-Tian Xie; Qing Dai; John M Kokontis; Catherine A Reardon; Godfrey S Getz; Shutsung Liao
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  British journal of pharmacology     Volume:  162     ISSN:  1476-5381     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-23     Completed Date:  2011-07-18     Revised Date:  2012-04-02    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1792-804     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
Affiliation:
Ben May Department for Cancer Research, University of Chicago, Chicago, IL, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Atherosclerosis / drug therapy*,  physiopathology
Cholesterol / blood,  metabolism
Dose-Response Relationship, Drug
Gene Expression Regulation / drug effects
Hydroxysteroids / administration & dosage,  adverse effects,  pharmacology*
Intestines / drug effects,  metabolism
Liver / drug effects,  metabolism
Macrophages / drug effects,  metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Orphan Nuclear Receptors / agonists*
Receptors, LDL / genetics*
Triglycerides / blood,  metabolism
Grant Support
ID/Acronym/Agency:
AT00850/AT/NCCAM NIH HHS; CA58073/CA/NCI NIH HHS; R01 CA058073-19/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/ATI-111 cpd; 0/Hydroxysteroids; 0/Orphan Nuclear Receptors; 0/Receptors, LDL; 0/Triglycerides; 0/liver X receptor; 57-88-5/Cholesterol

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