The role of postprandial releases of insulin and incretin hormones in meal-induced satiety - effect of obesity and weight reduction

BACKGROUND: Previous studies have indicated that the secretion of the intes tinal satiety hormone glucagon-like peptide-1 (GLP-1) is attenuated in obes e subjects. OBJECTIVE: To compare meal-induced response of GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) in obese and lean male subjects, to invest igate the effect of a major weight reduction in the obese subjects, and to look for an association between these hormones and ad libitum food intake. METHOD: Plasma concentrations of intestinal hormones and appetite sensation s were measured prior to, and every 30 min for 180 min after, ingestion of a 2.5 MJ solid test meal. Gastric emptying was estimated scintigraphically. An ad libitum lunch was served 3h after the test meal. SUBJECTS: Nineteen non-diabetic obese (body mass index (BMI) 34.1 -43.8 kg/ m(2)) and 12 lean (BMI 20.4-24.7 kg/m(2)) males. All obese subjects were re -examined after a mean stabilised weight loss of 18.8 kg (95% CI 14.4 -23.2 ). RESULTS: Total area under the GLP-1 response curve (AUC(total.GLP-1)) was l ower in obese before and after the weight loss compared to lean subjects (P < 0.05), although weight loss improved the response from 80 to 88% of that of the lean subjects (P = 0.003). The GIP response was similar in obese an d lean subjects. However, after the weight loss both AUC(total.GIP) and AUC (incremental),(GIP) were lowered (P < 0.05). An inverse correlation was obs erved between AUC(incremental, GIP) and energy intake at the subsequent ad libitum meal in all groups. In lean subjects ad libitum energy intake was l argely predicted by the insulin response to the preceding meal (r(2) = 0.67 , P = 0.001). CONCLUSION: Our study confirmed previous findings of a reduced postprandial GLP-1 response in severely obese subjects. Following weight reduction, GLP -1 response in the obese subjects apparently rose to a level between that o f obese and lean subjects. The data suggests that postprandial insulin and GIP responses are key players in short-term appetite regulation.