Insulin resistance is independently associated with postprandial alterations of triglyceride-rich lipoproteins in type 2 diabetes mellitus

Objective - To evaluate the role of insulin resistance in development of postprandial dyslipidemia in type 2 diabetic patients in an experimental setting in which these patients were compared with nondiabetic subjects at similar glucose and insulin blood levels. Methods and Results - Eight type 2 diabetic patients in optimal blood glucose control and 7 control subjects ( aged 50.0 +/- 2.6 and 48.1 +/- 1.3 years; body mass index 28.3 +/- 1.2 and 25.6 +/- 1.1 kg/m(2); fasting plasma triglycerides 1.12 +/- 0.13 and 0.87 +/- 0.08 mmol/L, respectively; mean +/- SEM; NS) consumed a mixed meal during an 8-hour hyperinsulinemic glycemic clamp. Mean blood glucose during clamp was approximate to 7.8 mmol/L, and plasma insulin during the preprandial steady state was approximate to 480 pmol/L in both groups, that differed for insulin sensitivity (M/I value lower in diabetic subjects [1.65 +/- 0.30 and 3.42 +/- 0.60; P < 0.05]). Subjects with diabetes had higher postprandial levels of lipids and apolipoprotein B (apoB) in large very low-density lipoprotein (incremental area for triglycerides 1814 +/- 421 versus 549 +/- 153 μmol/ L x 6 hours; P < 0.05; cholesterol 694 +/- 167 versus 226 +/- 41 mumol/L x 6 hours; P < 0.05; apoB-48 6.3 +/- 1.0 versus 2.6 +/- 0.7 mg/L x 6 hours; P < 0.05; apoB-100 56.5 +/- 14.9 versus 26.2 +/- 11.0 mg/ L x 6 hours; NS). Basal lipoprotein lipase (LPL) activity before and after meal was higher in diabetic subjects, whereas postheparin LPL activity 6 hours after the meal was similar. Conclusions - Insulin resistance is also associated with postprandial lipoprotein abnormalities in type 2 diabetes after acute correction for hyperglycemia and hyperinsulinemia.