ABSTRACT
It has been postulated that glucose regulation is secondary to maintenance of normal basal insulin secretion. Serum glucose, insulin, and C-peptide levels were measured at fasting in 209 consecutive non-insulin-dependent diabetic patients and after glucose stimulation in 193 patients. The basal serum insulin C-peptide levels were not significantly different in control subjects (mean 22 +/- 8.8 microU/ml) and in patients with varying severity of diabetes (mean 24 +/- 9.6 microU/ml) except in the most severely diabetic group [fasting serum glucose greater than 350 mg/dl (19.4 mmol/L), mean 19 +/- 7 microU/ml]. In 39 patients who developed ketonuria without acidosis during follow-up, the mean basal serum insulin was 22 microU/ml during the episode of ketonuria, 21 microU/ml during the glucose tolerance test, and 25 microU/ml after glucose stimulation (statistically nonsignificant differences). Our data suggest that hyperglycemia compensates for beta-cell impairment so that basal insulin secretion usually stays above the threshold for ketoacidosis unless there is marked beta-cell impairment. Patients who fail to increase insulin in response to nutrient challenge are at risk of developing ketosis.
