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Journal of Lipid Research, Vol. 48, 1336-1342, June 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Evidence of increased secretion of apolipoprotein B-48-containing lipoproteins in subjects with type 2 diabetes

Jean-Charles Hogue^*, Benoît Lamarche, André J. Tremblay^*, Jean Bergeron^*, Claude Gagné^* and Patrick Couture^1,*

^* Lipid Research Center, Centre hospitalier de l'Université Laval Research Center, Québec, Canada
Institute on Nutraceuticals and Functional Foods, Laval University, Québec, Canada

Published, JLR Papers in Press, March 3, 2007.

¹ To whom correspondence should be addressed. e-mail: patrick.couture{at}crchul.ulaval.ca

Patients with type 2 diabetes have high levels of triglyceride-rich lipoproteins (TRLs), including apolipoprotein B-48 (apoB-48)-containing TRLs of intestinal origin, but the mechanism leading to overaccumulation of these lipoproteins remains to be fully elucidated. Therefore, the objective of this study was to examine the in vivo kinetics of TRL apoB-48 and VLDL, intermediate density lipoprotein (IDL), and LDL apoB-100 in type 2 diabetic subjects (n = 11) and nondiabetic controls (n = 13) using a primed-constant infusion of L-[5,5,5-D₃]leucine for 12 h in the fed state. Diabetic subjects had significantly higher fasting glycemia, higher fasting insulinemia, higher plasma triglyceride, and lower HDL-cholesterol levels than controls. Compared with controls, diabetic subjects had increased TRL apoB-48, VLDL apoB-100, and IDL apoB-100 pool sizes as a result of increased production rates (PRs) and reduced fractional catabolic rates of these lipoprotein subfractions. Furthermore, multiple linear regression analyses revealed that the diabetic/control status was an independent predictor of TRL apoB-48 PR and represented nearly 35% of its variance. These results suggest that the overaccumulation of TRLs seen in patients with type 2 diabetes is attributable to increased PRs of both intestinally derived apoB-48-containing lipoproteins and TRL apoB-100 of hepatic origin and to decreased catabolism of these subfractions.

Supplementary key words kinetic study • stable isotope • hypertriglyceridemia

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