AUGMENTED INSULIN RESPONSES TO GLUCOSE AFTER SECRETIN PRIMING IN DIABETIC SUBJECTS

Previous studies have indicated that in normal man secretin directly stimulated rapid insulin responses and also augmented insulin responses (2-fold) to subsequent 5-g glucose pulses. To determine whether this phenomenon is observed in adult onset diabetes, patients with diminished (group A; n = 6) or absent (group B; n = 8) insulin responses to glucose were evaluated. Group A diabetics had decreased (P < 0.005) early responses to glucose pulses before (PI) and after (P2) secretin priming [PI, 54 ± 35% (mean ± SD), percent response above basal within 5 min; P2, 115 ± 60%] compared to normals (PI, 274 ± 144%; P2, 580 ± 470%). However, they had augmented insulin output to P2 (P < 0.01) and exhibited an identical degree of improvement (group A, 2.5-fold; normals, 2-fold). Faster (P < 0.05) glucose disappearance rates paralleled the increased output. Group B diabetics had absent acute insulin responses to both PI and P2. However, the total insulin output over 60 min was increased (P < 0.05) after P2, suggesting that the augmentation effect was not limited solely to the early phase of insulin release. Diabetic subjects (n = 8) without secretin priming had identical acute insulin responses, glucose disappearance rates, and total insulin responses to Pi and P2. Acute insulin responses to secretin per se (15 U pulse plus 3-U/min infusion for 25 min) were indistinguishable in both diabetic groups and previously reported normals (group A, 270 ± 152%; group B, 239 ± 140%; normals, 251 ± 122%). Thus, both the direct and augmentation effects of secretin on insulin release are intact in diabetic subjects. These results are consistent with the concept that adult onset diabetes may be related to an isolated defect in the mechanism by which glucose stimulates insulin release. © 1979 by The Endocrine Society.