Mechanism of hypertriglyceridaemia in diabetic patients with fasting hyperglycaemia.

Several aspects of lipid metabolism were studied to define the mechanism of hypertriglyceridaemia in insulin-independent diabetic patients with fasting hyperglycaemia. Patients with insulin-independent diabetes were more obese (p < 0.001) and had a significantly (p < 0.001) higher mean (+/- SEM) fasting plasma triglyceride concentration (387 +/- 66 mg/dl) than did either insulin-dependent diabetics (133 +/- 11 mg/dl) or normal (73 +/- 1 mg/dl) subjects. Very low density lipoprotein secretion rate was also significantly (p < 0.01 - < 0.001) higher in patients with insulin-independent diabetes (14.65 +/- 1.37 mg/kg/h) as compared to 7.64 +/- 0.60 mg x kg/h and 9.86 +/- 0.75 mg/kg/h in normal subjects and patients with insulin-dependent diabetes, respectively. However, the relationship between plasma triglyceride concentration and very low density lipoprotein-triglyceride secretion was similar in diabetics and in normals. The diabetic groups had equivalent degrees of fasting and postprandial hyperglycaemia, and comparable elevations of fasting plasma nonesterified free fatty acid levels (insulin-independent = 0.72 +/- 0.07 mmol/L, insulin-dependent = 0.63 +/- 0.08 mmol/L). Postprandial plasma insulin concentrations, however, reached normal levels in insulin-independent diabetics and were higher (p < 0.001) than in insulin-dependent diabetics. Thus, hypertriglyceridaemia in insulin-independent diabetics with fasting hyperglycaemia was associated with increased hepatic very low density lipoprotein-triglyceride secretion, and normal plasma insulin levels. The lower triglyeride levels in the insulin-dependent diabetics is assumed to be due to their relative hypoinsulinaemia.