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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:590.)
© 2006 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics

Dick C. Chan; Gerald F. Watts; Minh N. Nguyen; P. Hugh R. Barrett

From Metabolic Research Center, School of Medicine and Pharmacology, University of Western Australia, Perth, Australia.

Correspondence to Professor Gerald F Watts, School of Medicine and Pharmacology, University of Western Australia, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847, Australia. E-mail gfwatts{at}cyllene.uwa.edu.au

Objective— We investigated the associations between plasma very-low-density lipoprotein (VLDL)–apolipoprotein (apo)C-III and apoA-V concentrations and the kinetics of VLDL–apoB-100 and VLDL triglycerides in 15 men. We also explored the relationship between these parameters of VLDL metabolism and VLDL–apoC-III kinetics.

Methods and Results— ApoC-III, apoB, and triglyceride kinetics in VLDL were determined using stable isotopes and multicompartmental modeling to estimate production rate (PR) and fractional catabolic rate (FCR). Plasma VLDL–apoC-III concentration was significantly and inversely associated with the FCRs of VLDL triglycerides (r=–0.610) and VLDL–apoB (r=–0.791), and positively correlated with the PR of VLDL–apoC-III (r=0.842). However, apoA-V concentration was not significantly associated with any of the kinetic variables. There was a significant association (P<0.01) between the PRs of VLDL triglycerides and VLDL–apoB (r=0.641), and between the FCRs of VLDL triglycerides and VLDL–apoB (r=0.737). In multiple regression analysis, plasma VLDL–apoC-III concentration was a significant predictor of VLDL triglyceride FCR (ß-coefficient=–0.575) and VLDL–apoB FCR (ß-coefficient=–0.839).

Conclusions— Our findings suggest that increased VLDL–apoC-III concentrations resulting from an overproduction of VLDL–apoC-III are strongly associated with the delayed catabolism of triglycerides and apoB in VLDL. We also demonstrated that the kinetics of VLDL triglycerides and apoB are closely coupled. Our data do not support a role for plasma apoA-V in regulating VLDL kinetics.

We investigated the associations between plasma VLDL-apoC-III and apoA-V concentrations and the kinetics of VLDL-apoB-100 and VLDL triglyceride in 15 men. Increased VLDL-apoC-III concentrations resulting from an overproduction of VLDL-apoC-III was a predictor of the delayed catabolism of VLDL triglyceride and VLDL-apoB. However, apo-V concentration was not significantly associated with VLDL kinetics.

Key Words: apoA-V • apoC-III • cardiovascular disease • lipoprotein metabolism

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