Document Detail

Chylomicron- and VLDL-derived lipids enter the heart through different pathways: in vivo evidence for receptor- and non-receptor-mediated fatty acid uptake.
MedLine Citation:
PMID:  20852327     Owner:  NLM     Status:  MEDLINE    
Lipids circulate in the blood in association with plasma lipoproteins and enter the tissues either after hydrolysis or as non-hydrolyzable lipid esters. We studied cardiac lipids, lipoprotein lipid uptake, and gene expression in heart-specific lipoprotein lipase (LpL) knock-out (hLpL0), CD36 knock-out (Cd36(-/-)), and double knock-out (hLpL0/Cd36(-/-)-DKO) mice. Loss of either LpL or CD36 led to a significant reduction in heart total fatty acyl-CoA (control, 99.5 ± 3.8; hLpL0, 36.2 ± 3.5; Cd36(-/-), 57.7 ± 5.5 nmol/g, p < 0.05) and an additive effect was observed in the DKO (20.2 ± 1.4 nmol/g, p < 0.05). Myocardial VLDL-triglyceride (TG) uptake was reduced in the hLpL0 (31 ± 6%) and Cd36(-/-) (47 ± 4%) mice with an additive reduction in the DKO (64 ± 5%) compared with control. However, LpL but not CD36 deficiency decreased VLDL-cholesteryl ester uptake. Endogenously labeled mouse chylomicrons were produced by tamoxifen treatment of β-actin-MerCreMer/LpL(flox/flox) mice. Induced loss of LpL increased TG levels >10-fold and reduced HDL by >50%. After injection of these labeled chylomicrons in the different mice, chylomicron TG uptake was reduced by ∼70% and retinyl ester by ∼50% in hLpL0 hearts. Loss of CD36 did not alter either chylomicron TG or retinyl ester uptake. LpL loss did not affect uptake of remnant lipoproteins from ApoE knock-out mice. Our data are consistent with two pathways for fatty acid uptake; a CD36 process for VLDL-derived fatty acid and a non-CD36 process for chylomicron-derived fatty acid uptake. In addition, our data show that lipolysis is involved in uptake of core lipids from TG-rich lipoproteins.
Kalyani G Bharadwaj; Yaeko Hiyama; Yunying Hu; Lesley Ann Huggins; Rajasekhar Ramakrishnan; Nada A Abumrad; Gerald I Shulman; William S Blaner; Ira J Goldberg
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-09-18
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  285     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-29     Completed Date:  2010-12-30     Revised Date:  2014-09-18    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  37976-86     Citation Subset:  IM    
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MeSH Terms
Antigens, CD36 / genetics,  metabolism*
Antineoplastic Agents, Hormonal / pharmacokinetics
Cholesterol, VLDL / genetics,  metabolism*
Chylomicrons / genetics,  metabolism*
Fatty Acids / genetics,  metabolism*
Lipid Metabolism / drug effects,  physiology*
Lipoprotein Lipase / genetics,  metabolism*
Lipoproteins, VLDL / genetics,  metabolism*
Mice, Knockout
Myocardium / metabolism*
Tamoxifen / pharmacology
Triglycerides / genetics,  metabolism*
Grant Support
AA019413/AA/NIAAA NIH HHS; DK079221/DK/NIDDK NIH HHS; HL45095/HL/NHLBI NIH HHS; HL73029/HL/NHLBI NIH HHS; P01 HL057278/HL/NHLBI NIH HHS; P30 DK034989/DK/NIDDK NIH HHS; P30 DK056341/DK/NIDDK NIH HHS; P30 DK056341-10/DK/NIDDK NIH HHS; R01 DK033301/DK/NIDDK NIH HHS; R01 DK040936/DK/NIDDK NIH HHS; R01 HL045095/HL/NHLBI NIH HHS; R01 HL073029/HL/NHLBI NIH HHS; U24 DK059635/DK/NIDDK NIH HHS; //Howard Hughes Medical Institute
Reg. No./Substance:
0/Antigens, CD36; 0/Antineoplastic Agents, Hormonal; 0/Cholesterol, VLDL; 0/Chylomicrons; 0/Fatty Acids; 0/Lipoproteins, VLDL; 0/Triglycerides; 0/very low density lipoprotein triglyceride; 094ZI81Y45/Tamoxifen; EC Lipase

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