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

Jean-Charles Hogue, Benoit Lamarche, André J. Tremblay, Jean Bergeron, Claude Gagné, and Patrick Couture

Medicine, Laval University Medical Center, Quebec City, Quebec G1V 4G2

Corresponding Author: patrick.couture{at}crchul.ulaval.ca

Patients with type 2 diabetes have high levels of triglyceride-rich lipoproteins (TRL), including apolipoprotein (apo) B-48-containing TRL 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, IDL and LDL apoB-100 in type 2 diabetic subjects (n=11) and non-diabetic controls (n=13) using a primed-constant infusion of [5,5,5-D3]-L-leucine for 12 hours in the fed state. Diabetic subjects had significantly higher fasting glycemia, higher fasting insulinemia, higher plasma triglyceride (TG) and lower HDL-C levels than controls. As compared with controls, diabetic subjects had increased TRL apoB-48, VLDL apoB-100 and IDL apoB-100 pool sizes due to elevated production rates (PR) 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 overaccumulation of TRL seen in patients with type 2 diabetes is due to increased production rate of both intestinally derived apoB-48-containing lipoproteins and TRL apoB-100 of hepatic origin and to decreased catabolism of these subfractions.

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