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Papers In Press, published online ahead of print September 16, 2002
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Submitted on May 29, 2002
Department of Medicine, Columbia University, New York, NY 10032
Corresponding Author: nss5{at}columbia.edu
Apolipoprotein (apo) C-I has been proposed to act primarily via interference with apoE-mediated lipoprotein uptake. To define actions of apoC-I that are independent of apoE, we crossed a moderately overexpressing human apoC-I transgenic, which possesses a minimal phenotype in the WT background, with the apoE-null mouse. Surprisingly, apoE-null/C-I mice showed much more severe hyperlipidemia than apoE-null littermates in both the fasting and non-fasting states, with an almost doubling of cholesterol, primarily in IDL+LDL, and a marked increase in triglycerides, 3-fold in females to 260 ± 80 mg/dl and 14-fold in males to 1409 ± 594 mg/dl. HDL lipids were not significantly altered but HDL were apoC-I-enriched and apoA-II-depleted. Production rates of VLDL triglyceride were unchanged as was the clearance of post-lipolysis remnant particles. Plasma post-heparin hepatic lipase and lipoprotein lipase levels were undiminished as was the in vitro hydrolysis of apoC-I transgenic VLDL. However, HDL from apoC-I transgenic mice had a marked inhibitory effect on hepatic lipase activity, as did purified apoC-I. LPL activity was minimally affected. Atherosclerosis assay revealed significantly increased atherosclerosis in apoE-null/C-I mice assessed via the en face assay. Inhibition of hepatic lipase may be an important mechanism of the decrease in lipoprotein clearance mediated by apoC-I.
Revised on September 6, 2002
Accepted on September 16, 2002
Overexpression of apolipoprotein C-I in apolipoprotein E-null mice: Severe hypertriglyceridemia due to inhibition of hepatic lipase
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