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 μU/ml) and in patients with varying severity of diabetes (mean 24 ± 9.6 μU/ml) except in the most severely diabetic group [fasting serum glucose >350 mg/dl (19.4 mmol/L), mean 19± 7 μU/ml]. In 39 patients who developed ketonuria without acidosis during follow-up, the mean basal serum insulin was 22 μU/ml during the episode of ketonuria, 21 μU/ml during the glucose tolerance test, and 25 μU/ml after glucose stimulation (statistically nonsignificant differences). Our data suggest that hyperglycemia compensates for β-cell impairment so that basal insulin secretion usually stays above the threshold for ketoacidosis unless there is marked β-cell impairment. Patients who fail to increase insulin in response to nutrient challenge are at risk of developing ketosis.

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