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Originally published In Press as doi:10.1194/jlr.M600384-JLR200 on October 3, 2006

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Journal of Lipid Research, Vol. 48, 145-151, January 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Reduction of plasma triglycerides in apolipoprotein C-II transgenic mice overexpressing lipoprotein lipase in muscle

Leslie K. Pulawa, Dalan R. Jensen, Alison Coates1 and Robert H. Eckel2

Division of Endocrinology, Metabolism, and Diabetes, University of Colorado at Denver and Health Sciences Center, Aurora, CO

Published, JLR Papers in Press, October 3, 2006.

1 Present address of A. Coates: Nutritional Physiology Research Centre, School of Health Sciences, University of South Australia, Adelaide, South Australia, Australia.

2 To whom correspondence should be addressed. e-mail: robert.eckel{at}uchsc.edu

LPL and its specific physiological activator, apolipoprotein C-II (apoC-II), regulate the hydrolysis of triglycerides (TGs) from circulating TG-rich lipoproteins. Previously, we developed a skeletal muscle-specific LPL transgenic mouse that had lower plasma TG levels. ApoC-II transgenic mice develop hypertriglyceridemia attributed to delayed clearance. To investigate whether overexpression of LPL could correct this apoC-II-induced hypertriglyceridemia, mice with overexpression of human apoC-II (CII) were cross-bred with mice with two levels of muscle-specific human LPL overexpression (LPL-L or LPL-H). Plasma TG levels were 319 ± 39 mg/dl in CII mice and 39 ± 5 mg/dl in wild-type mice. Compared with CII mice, apoC-II transgenic mice with the higher level of LPL overexpression (CIILPL-H) had a 50% reduction in plasma TG levels (P = 0.013). Heart LPL activity was reduced by ~30% in mice with the human apoC-II transgene, which accompanied a more modest 10% decrease in total LPL protein. Overexpression of human LPL in skeletal muscle resulted in dose-dependent reduction of plasma TGs in apoC-II transgenic mice. Along with plasma apoC-II concentrations, heart and skeletal muscle LPL activities were predictors of plasma TGs. These data suggest that mice with the human apoC-II transgene may have alterations in the expression/activity of endogenous LPL in the heart. Furthermore, the decrease of LPL activity in the heart, along with the inhibitory effects of excess apoC-II, may contribute to the hypertriglyceridemia observed in apoC-II transgenic mice.

Supplementary key words hypertriglyceridemia • lipid metabolism • heparin-releasable lipoprotein lipase activity • heart • fasting

Abbreviations: apoC-II, apolipoprotein C-II; HSPG, heparan sulfate proteoglycan; TG, triglyceride; WT, wild-type


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