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The effect of dietary modification and hyperglycaemia on gastric emptying and gastric inhibitory polypeptide (GIP) secretion

1. Five healthy volunteers whose usual fat and energy intakes were moderately high (fat intake 155 (SE 11) g/d; energy intake 13683 (SE 909) kJ/d) were given on two separate occasions (a) 96 g fat and (b) 96 g fat and intravenous (IV) glucose (250 g glucose/1; 100 ml followed by a 2 ml/min infusion for 180 min). 2. Subjects continued on a low-fat diet for 35 d (fat intake 25 (SE 4) g/d; energy intake 6976 (SE 539) kJ/d) and the tests repeated. 3. The gastric inhibitory polypeptide (GIP) response to oral fat was significantly attenuated by IV glucose whilst subjects were consuming their normal diets and the GIP response to fat alone was significantly diminished during the low-fat diet. Post-prandial plasma triglycerides, light scattering indices (LSI; an index of post-prandial chylomicronaemia) and paracetamol levels paralleled the integrated GIP responses on both normal and low-fat diets. 4. The study of oral fat with or without glucose was repeated on seven further volunteers consuming their usual diet, substituting 10 MBq 99Tcm-labelled tin colloid for the paracetamol to investigate the rate of gastric emptying by radionuclide imaging. 5. Plasma GIP, insulin, triglyceride and LSI levels were similar to those found in the first study. IV glucose almost doubled the gastric emptying time of the oral fat load (half emptying time (t½) 148 (SE 11) min after fat alone and 224 (SE 18) min after fat and IV glucose). Post-prandial plasma motilin levels were significantly depressed by IV glucose. 6. We conclude that (a) the GIP response to oral fat is attenuated both by IV glucose and by a low-fat diet, (b) the delay in gastric emptying induced by IV glucose may be partly responsible for the diminished GIP response to oral fat when IV glucose is infused, (c) it is possible that some of the changes observed with IV glucose are mediated via changes in motilin.