High glucose levels do not directly impair cellular binding of HDL3 or HDL-mediated efflux of cholesterol from human skin fibroblasts.

The excess risk of atherosclerosis that is associated with diabetes mellitus cannot be completely accounted for by other known risk factors. Recent studies have suggested that increased glycation of high density lipoproteins (HDL) at high glucose concentrations causes functional abnormalities that might contribute to accelerated atherosclerosis. Other investigators also have shown that elevated glucose concentrations can stimulate the activity of protein kinase C in cultured cells. Because protein kinase C appears to be involved in HDL receptor-mediated efflux, the hypothesis that a high glucose concentration in vitro might modulate HDL-mediated efflux of cholesterol from human fibroblasts was tested. These studies indicate that a high glucose level alone does not affect the interaction of normal HDL3 with cultured human skin fibroblasts.