| CD36 deficiency impairs intestinal lipid secretion and clearance of chylomicrons from the blood. | |
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MedLine Citation:
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PMID: 15841205 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CD36 mediates the transfer of fatty acids (FAs) across the plasma membranes of muscle and adipose cells, thus playing an important role in regulating peripheral FA metabolism in vivo. In the proximal intestine, CD36 is localized in abundant quantities on the apical surface of epithelial cells, a pattern similar to that of other proteins implicated in the uptake of dietary FAs. To define the role of CD36 in the intestine, we examined FA utilization and lipoprotein secretion by WT and CD36-null mice in response to acute and chronic fat feeding. CD36-null mice given a fat bolus by gavage or fed a high-fat diet accumulated neutral lipid in the proximal intestine, which indicated abnormal lipid processing. Using a model in which mice were equipped with lymph fistulae, we obtained evidence of defective lipoprotein secretion by directly measuring lipid output. The secretion defect appeared to reflect an impaired ability of CD36-null enterocytes to efficiently synthesize triacylglycerols from dietary FAs in the endoplasmic reticulum. In the plasma of intact mice, the reduced intestinal lipid secretion was masked by slow clearance of intestine-derived lipoproteins. The impaired clearance occurred despite normal lipoprotein lipase activity and likely reflected feedback inhibition of the lipase by FAs due to their defective removal from the plasma. We conclude that CD36 is important for both secretion and clearance of intestinal lipoproteins. CD36 deficiency results in hypertriglyceridemia both in the postprandial and fasting states and in humans may constitute a risk factor for diet-induced type 2 diabetes and cardiovascular disease. |
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Authors:
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Victor A Drover; Mohammad Ajmal; Fatiha Nassir; Nicholas O Davidson; Andromeda M Nauli; Daisy Sahoo; Patrick Tso; Nada A Abumrad |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S. Date: 2005-04-07 |
Journal Detail:
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Title: The Journal of clinical investigation Volume: 115 ISSN: 0021-9738 ISO Abbreviation: J. Clin. Invest. Publication Date: 2005 May |
Date Detail:
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Created Date: 2005-05-02 Completed Date: 2005-07-12 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7802877 Medline TA: J Clin Invest Country: United States |
Other Details:
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Languages: eng Pagination: 1290-7 Citation Subset: AIM; IM |
Affiliation:
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Department of Physiology and Biophysics, State University of New York at Stony Brook, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, CD36 / genetics, metabolism* Apolipoproteins C / biosynthesis, genetics Chylomicrons / blood* Enterocytes / metabolism Fatty Acids / metabolism Intestine, Small / metabolism*, pathology, secretion Lipids / secretion* Mice Mice, Inbred C57BL RNA, Messenger / metabolism Time Factors Triglycerides / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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DK 56260/DK/NIDDK NIH HHS; DK 600220/DK/NIDDK NIH HHS; DK33301/DK/NIDDK NIH HHS; HL-38180/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD36; 0/Apolipoproteins C; 0/Chylomicrons; 0/Fatty Acids; 0/Lipids; 0/RNA, Messenger; 0/Triglycerides |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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