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Journal of Lipid Research, Vol. 46, 2175-2181, October 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

CD36 deficiency in mice impairs lipoprotein lipase-mediated triglyceride clearance

Jeltje R. Goudriaan^1,*, Marion A. M. den Boer^1,*,, Patrick C. N. Rensen^*,, Maria Febbraio^**, Folkert Kuipers, Johannes A. Romijn, Louis M. Havekes^*, and Peter J. Voshol^2,*,

^* Netherlands Organization for Applied Scientific Research-Quality of Life, Gaubius Laboratory, Leiden, The Netherlands
Department of Endocrinology and Diabetes, Leiden University Medical Center, Leiden, The Netherlands
Department of Cardiology and General Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands
^** Division of Hematology/Oncology, Cornell University, New York, NY
Laboratory of Pediatrics, Center for Liver, Digestive, and Metabolic Diseases, University Hospital Groningen, Groningen, The Netherlands

Published, JLR Papers in Press, July 16, 2005. DOI 10.1194/jlr.M500112-JLR200

¹ J. R. Goudriaan and M. A. M. den Boer contributed equally to this work.

² To whom correspondence should be addressed. e-mail: p.j.voshol{at}lumc.nl

CD36 is involved in high-affinity peripheral FFA uptake. CD36-deficient (cd36^–/–) mice exhibit increased plasma FFA and triglyceride (TG) levels. The aim of the present study was to elucidate the cause of the increased plasma TG levels in cd36^–/– mice. cd36^–/– mice showed no differences in hepatic VLDL-TG production or intestinal [³H]TG uptake compared with wild-type littermates. cd36^–/– mice showed a 2-fold enhanced postprandial TG response upon an intragastric fat load (P < 0.05), with a concomitant 2.5-fold increased FFA response (P < 0.05), suggesting that the increased FFA in cd36^–/– mice may impair LPL-mediated TG hydrolysis. Postheparin LPL levels were not affected. However, the in vitro LPL-mediated TG hydrolysis rate as induced by postheparin plasma of cd36^–/– mice in the absence of excess FFA-free BSA was reduced 2-fold compared with wild-type plasma (P < 0.05). This inhibition was relieved upon the addition of excess FFA-free BSA. Likewise, increasing plasma FFA in wild-type mice to the levels observed in cd36^–/– mice by infusion prolonged the plasma half-life of glycerol tri[³H]oleate-labeled VLDL-like emulsion particles by 2.5-fold (P < 0.05).

We conclude that the increased plasma TG levels observed in cd36^–/– mice are caused by decreased LPL-mediated hydrolysis of TG-rich lipoproteins resulting from FFA-induced product inhibition of LPL.

Abbreviations: apoC-I, apolipoprotein C-I; AUC_{0–8.5 h}, area under the curve at 0–8.5 h; cd36^–/–, CD36-deficient; TG, triglyceride

Supplementary key words free fatty acids • fatty acid transport • postprandial lipid metabolism • transgenic mice • triglyceride hydrolysis

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