Diabetic subjects have previously been found to have increased secretion of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to oral glucose or triglyceride compared with normal subjects. In the present study, a group of 19 diabetics was selected with milder glucose intolerance (fasting plasma glucose = 109 mg. per deciliter) than those reported previously. In these diabetics no enhancement of IRGIP responses was found to either 75 gm. oral glucose or 50 ml. oral corn oil when compared with 13 subjects with normal carbohydrate tolerance. Some of the subjects were obese and, when assessed independently from glucose tolerance, obesity was associated with higher integrated IRGIP responses to oral glucose but not to oral corn oil. The degree of obesity (92 to 154 per cent ideal body weight) did not correlate with fasting or stimulated IRGIP responses of the 32 subjects. One hour after ingestion of 50 ml. corn oil, when IRGIP concentrations were maximal but glucose and insulin remained unaffected, the diabetic subjects showed increased relative acute-phase insulin secretion to a 20 gm. pulse of intravenous glucose compared with that from a glucose pulse alone (p < 0.01). Subjects with normal carbohydrate tolerance had no increase in relative acute insulin response to glucose after triglyceride priming. The relative second-phase insulin response (10 to 30 min.) increased significantly with triglyceride priming in both diabetics (p < 0.01) and nondiabetics (p < 0.05). Although glucose disappearance rates (Kg) correlated with relative insulin responses, the increase in insulin secretion with triglyceride priming was not associated with an increase in Kg. Although obese subjects show increased stimulated GIP responses to oral glucose, patients with mild diabetes have normal GIP secretion to oral glucose and to triglyceride, but show a GIP-associated increase in both phases of glucose-induced insulin secretion.

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