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To test whether monocyte-derived macrophages obtained from diabetic patients with hypertriglyceridemia have an altered manner of lipid accumulation, we separated monocytes from 7 healthy control subjects, 9 diabetic normolipidemic patients, 9 diabetic hypertriglyceridemic patients, and 7 nondiabetic hypertriglyceridemic patients. The monocytes of each group were modulated to macrophages under two different culture systems using either autologous serum or heterologous normal non-diabetic non-hypertriglyceridemic serum in the culture medium.The cells transformed better in the healthy serum system. In this system, the [14C] oleate incorporation into cholesterol oleate by macrophages derived from the diabetic group (0.30±0.11nmol/mg protein/12h (mean±SD), p<0.05) and diabetic-hypertriglyceridemic group (0.40±0.12nmol/mg protein/12h, p<0.005) was significantly higher than that by macrophages derived from the hypertriglyceridemic group (0.21±0.16nmol/mg protein/12h) and healthy group (0.22±0.02nmol/mg protein/12h). With the autologous serum system, similar results were obtained, although there was more fluctuation of the values within a group. When the degradation of labeled lipoproteins in the macrophages was determined concomitantly, the macrophages from all four groups degraded 125I-acetyl LDL equally; however the rates of 125I-labeled “hypertriglyceridemic” VLDL degradation were significantly lower by macrophages from the diabetic group (8.9±3.5μg/mg protein/12h, p<0.05) and the diabetic-hypertriglyceridemic group (8.1±1.2μg/mg protein/12h, p<0.01) than by those from healthy group (12.4±2.6μg/mg protein/12h) and hypertriglyceridemic group (11.4±3.7μg/mg protein/12h) grown in the healthy serum culture system.Macrophages from diabetic patients may have accelerated cholesterol esterification because of the lowered VLDL influx. The increase was strongly linked with the diabetic condition and was not unique to the diabetic-hypertriglyceridemic patients. This trend may accelerate atherosclerosis in diabetic hypertriglyceridemia when an atherogenic factor specific to hypertriglyceridemia coexists.

Enhanced Cholesterol Esterification in Monocyte-Derived Macrophages from Diabetic But Not Hypertriglyceridemic Men.