To determine whether compositional abnormalities are present in high-density lipoprotein (HDL) in patients with insulin-dependent diabetes mellitus (IDOM) that might negate its putatively protective cardiovascular effects, we studied the plasma lipoproteins of 12 men with varying degrees of clinical control (mean fasting glucose 193 ± 10 mg/dl, mean glycoalbumin > 73% above control mean). The diabetic patients' basal plasma triglyceride, total- and free- (unesterified) cholesterol, HDL cholesterol (HDL-chol), and apolipoprotein Al, All, and B concentrations were similar to those of control subjects, but the freecholesterol- to-lecithin ratio, a new index of cardiovascular disease risk, was significantly increased in their plasma (0.97 ± 0.14 vs. 0.88 ± 0.07, P < .02) and their very-low-density lipoprotein (VLDL)-low-density lipoprotein (LDL) subfraction (1.50 ± 0.51 vs. 1.08 ± 0.15, P < .005). Although HDL2-chol was similar in diabetic and control groups, the HDL2-chol-to-free-cholesterol ratio (diabetic vs. control, 4.64 ± 1.7 vs. 1.96 ± 1.0 μmol/ml, P < .025) and the sphingomyelin-to-lecithin ratio (0.23 ± 0.08 vs. 0.20 ± 0.09, P < .025) were both significantly increased in the IDDM group. HDL3-chol was higher in the IDDM than in the control subjects (diabetic vs. control, 38.6 ± 5.2 vs. 32.7 ± 2.7 mg/dl, P < .005). In contrast to whole plasma and the VLDL + LDL subfraction, the freecholesterol- to-lecithin ratio of IDDM and control HDL subfractions were similar. These results demonstrate that men with IDDM have both qualitative and quantitative changes in lipoprotein surface lipid composition involving VLDL + LDL and HDL2 plasma subfractions. Because changes in the amounts of free cholesterol and phospholipid in lipoproteins have been shown to influence the directional fluxes of cholesterol, these compositional alterations suggest that IDDM may adversely affect both lipoproteinlipoprotein and lipoprotein-cell interactions.

This content is only available via PDF.