The Increase of Apolipoprotein A-V During Postprandial Lipemia Parallels the Response of Triglyceride-Rich Lipoproteins in Type 2 Diabetes: No relationship between apoA-V and postheparin plasma lipolytic activity

Postprandial lipemia is a distinct feature of diabetic dyslipidemia and may partly explain the atherogeneity of the lipid profile in type 2 diabetes (1). Several genetic factors contribute to the elevation of triglyceride-rich lipoproteins (TRLs). The role of apolipoprotein (apo)C-III as a regulator of TRL metabolism is well documented (2). Recently, apoA-V has been identified as a novel regulator of triglyceride metabolism. When the human APOA5 gene was expressed in transgenic mice, plasma triglyceride concentration was decreased by 70%, whereas apoA 5 gene knockout mice had fourfold elevation of plasma triglyceride levels (3). Inherited apoA-V deficiency results in severe hypertriglyceridemia in humans (4). A mutation in the APOA5 gene causes hypertriglyceridemia due to decreased lipoprotein lipase (LPL) mass and activity (5). Thus, previous studies have proposed that apoA-V decreases triglycerides by stimulating lipolysis. The present study focused on the response of apoA-V and apoC-III during postprandial lipemia and the associations between apoA-V and apoC-III and postheparin plasma LPL and hepatic lipase activities in type 2 diabetes. The present study cohort was comprised of 39 men and 8 women with type 2 diabetes who were enrolled in the previously published nateglinide study with the same inclusion and exclusion criteria (6). A total of 17 patients were treated with diet alone, 20 with sulfonylurea, and 11 with metformin. The …