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PMID: 11368757 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Down-regulation of intestinal scavenger receptor class B, type I (SR-BI) expression in rodents under conditions of deficient bile delivery to the intestine.

The Biochemical journal ·Vol. 356 ·No. Pt 2 ·2001-06-01 ·Pages 317-25

Voshol PJ, Schwarz M, Rigotti A, Krieger M, Groen AK, Kuipers F

Abstract

Scavenger receptor class B, type I (SR-BI) is expressed in the intestines of rodents and has been suggested to be involved in the absorption of dietary cholesterol. The aim of this study was to determine whether intestinal SR-BI expression is affected in animal models with altered bile delivery to the intestine and impaired cholesterol absorption. SR-BI protein and mRNA levels were determined in proximal and distal small intestine from control, bile-duct-ligated and bile-diverted rats and from control and bile-duct-ligated mice. Two genetically altered mouse models were studied: multidrug resistance-2 P-glycoprotein-deficient [Mdr2((-/-))] mice that produce phospholipid/cholesterol-free bile, and cholesterol 7alpha-hydroxylase-deficient [Cyp7a((-/-))] mice, which exhibit qualitative and quantitative changes in the bile-salt pool. Cholesterol-absorption efficiency was quantified using a dual-isotope ratio method. SR-BI was present at the apical membrane of enterocytes in control rats and mice and was more abundant in proximal than in distal segments of the intestine. In bile-duct-ligated animals, levels of SR-BI protein were virtually absent and mRNA levels were decreased by approximately 50%. Bile-diverted rats, Mdr2((-/-)) mice and Cyp7a((-/-)) mice showed decreased levels of intestinal SR-BI protein while mRNA levels were unaffected. Cholesterol absorption was reduced by >90% in bile-duct-ligated and bile-diverted animals and in Cyp7a((-/-)) mice, whereas Mdr2((-/-)) mice showed an approximately 50% reduction. This study shows that SR-BI is expressed at the apical membrane of enterocytes of rats and mice, mainly in the upper intestine where cholesterol absorption is greatest, and indicates that bile components play a role in post-transcriptional regulation of SR-BI expression. Factors associated with cholestasis appear to be involved in transcriptional control of intestinal SR-BI expression. The role of SR-BI in the cholesterol-absorption process remains to be defined.

MeSH Terms
ATP Binding Cassette Transporter, Subfamily B/genetics ATP-Binding Cassette Transporters/genetics Animals Base Sequence Bile/metabolism Bile Ducts CD36 Antigens/genetics,metabolism Cholesterol/metabolism Cholesterol 7-alpha-Hydroxylase/deficiency,genetics DNA Primers/genetics Down-Regulation Enterohepatic Circulation Intestinal Absorption Intestinal Mucosa/metabolism Ligation Male Membrane Proteins Mice Mice, Inbred C57BL Mice, Knockout RNA, Messenger/genetics,metabolism Rats Rats, Wistar Receptors, Immunologic Receptors, Lipoprotein Receptors, Scavenger Reverse Transcriptase Polymerase Chain Reaction Scavenger Receptors, Class B
Chemicals
ATP Binding Cassette Transporter, Subfamily B ATP-Binding Cassette Transporters CD36 Antigens DNA Primers Membrane Proteins RNA, Messenger Receptors, Immunologic Receptors, Lipoprotein Receptors, Scavenger Scarb1 protein, mouse Scarb1 protein, rat Scavenger Receptors, Class B Cholesterol multidrug resistance protein 3 Cholesterol 7-alpha-Hydroxylase
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Voshol P J
Groningen University Institute for Drug Exploration, Center for Liver, Digestive and Metabolic Diseases, University Hospital Groningen, Hanzeplein 1, NL-9713 GZ Groningen, The Netherlands.
Schwarz M
Rigotti A
Krieger M
Groen A K
Kuipers F
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Article Info
Journal
The Biochemical journal
Abbr.
Biochem J
ISSN
0264-6021
DOI
10.1042/0264-6021:3560317
Published
2001-06-01
Pages
317-25
Language
English
Region
England
NLM ID
2984726R
PMCID
PMC1221841
Subset
IM
Grants
NHLBI NIH HHS · HL20948 · United States
NHLBI NIH HHS · HL52212 · United States
NHLBI NIH HHS · HL41484 · United States
NIDDK NIH HHS · 5-T32-DK07745 · United States
NHLBI NIH HHS · HL64737 · United States
External Links
PubMed source DOI: 10.1042/0264-6021:3560317 PMC Full Text View journal details
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