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Plasma lipid concentration and lipoprotein composition were studied before and after several months of glipizide treatment in 23 patients with non-insulin-dependent diabetes mellitus. The mean (+/- SEM) plasma glucose level fell 87 mg/dL, and the fall in plasma glucose concentration was correlated with a reduction in plasma triglyceride, very low-density lipoprotein triglyceride, cholesterol, and low-density lipoprotein cholesterol levels. Furthermore, there was a statistically significant increase in the plasma high-density lipoprotein cholesterol to total cholesterol ratio. Thus, improved diabetic control in patients treated with glipizide with non-insulin-dependent diabetes mellitus leads to changes in lipoprotein metabolism thought to be beneficial in terms of known cardiovascular risk factors.

The effect of age on glucose tolerance, insulin secretion, and in vivo insulin action (insulin clamp) was studied in 48 nonobese subjects, all of whom were fully ambulatory and in good general health. The observed age-related increase in fasting plasma glucose (r = 0.35, P less than 0.01) was not due to an increase in relative body weight (RBW). Plasma insulin levels, both fasting and postprandial, tended to rise with age, but these changes were not significant. There was a marginally significant correlation (r = -0.21) between age and insulin-stimulated glucose utilization, which fell to -0.13 when controlled for RBW. However, steady-state insulin levels during the insulin-clamp period were higher in the older subjects, suggesting that age leads to an impairment in insulin catabolism; thus it is likely that the impairment of in vivo insulin action with age was underestimated. The variation in in vivo action between individuals was much greater among the older subjects. It was concluded that the glucose intolerance associated with aging is of relatively minor magnitude when ambulatory, generally healthy, nonobese, and nondiabetic subjects are studied. The cause of the glucose intolerance associated with aging seems to be loss of normal in vivo insulin action. On the other hand, this defect is not shared by all older persons, and in many over the age of 70, glucose transport is as efficient as in persons in their 20s.