Augmented gastric inhibitory polypeptide and insulin responses to a meal after an increase in carbohydrate (sucrose) intake.

The gastric inhibitory polypeptide (GIP) response to certain stimuli may be exaggerated in patients with obesity and noninsulin-dependent diabetes mellitus. To explore the effects of increased caloric intake and dietary composition on GIP secretion, 20 normal lean volunteers underwent a 4-week ambulatory study. A baseline week (usual diet) was followed by 3 weeks in which the usual diet was supplemented with 45 g fat (diet A), 100 g carbohydrate in the form of sucrose (diet B), or 50 g protein (diet C) for 1 week each. Almost equal numbers of subjects followed sequence ABC, BCA, or CAB in this cross-over study. At the end of the baseline week and each study week, serum glucose, insulin, and GIP were measured in response to a 500-cal liquid test meal. Daily intake of carbohydrate, protein, or fat, as monitored by food records, increased significantly (P less than 0.01) during the appropriate dietary periods, whereas body weight changed slightly, but not significantly, during the 3 study periods. No changes occurred in the total integrated serum glucose concentrations, whereas integrated insulin concentrations changed significantly (P less than 0.05), being 32.5 +/- 3.1 (+/- SEM), 37.2 +/- 4.0, and 30.3 +/- 3.1 microU/ml min-1 during periods A, B, and C, respectively. Insulin secretion was greatest during period B, the carbohydrate week, when insulin concentrations 15-60 min after the test meal were significantly greater (P less than 0.05 to P less than 0.01) than after the baseline period. Total integrated incremental serum GIP concentrations were also significantly different (P less than 0.01) during the 3 study periods, being 1.93 +/- 0.13, 2.53 +/- 0.24, and 1.90 +/- 0.11 ng/ml min-1 during A, B, and C, respectively. Serum GIP was highest during period B (carbohydrate), when average concentrations were significantly higher (P less than 0.01) 15-60 min after the meal compared to those during the baseline study. Similar changes did not occur with the other diets. Thus, GIP and insulin secretion were substantially altered by an acute increase in sucrose intake. The exaggerated GIP response to a meal in some patients with obesity may possibly be the result of adaptation of intestinal GIP cells to diet, particularly one rich in sucrose.