Ingestion of fat before a carbohydrate meal markedly slows GE and attenuates the postprandial rises in glucose, insulin, and GIP, but stimulates GLP-1, in type 2 diabetes.

Load-dependent effects of duodenal glucose on glycemia, gastrointestinal hormones, antropyloroduodenal motility, and energy intake in healthy men. Am J Physiol Endocrinol Metab 293: E743-E753, 2007. First published July 3, 2007; doi:10.1152/ajpendo.00159.2007.-Gastric emptying is a major determinant of glycemia, gastrointestinal hormone release, and appetite. We determined the effects of different intraduodenal glucose loads on glycemia, insulinemia, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin (CCK), antropyloroduodenal motility, and energy intake in healthy subjects. Blood glucose, plasma hormone, and antropyloroduodenal motor responses to 120-min intraduodenal infusions of glucose at 1) 1 ("G1"), 2) 2 ("G2"), and 3) 4 ("G4") kcal/min or of 4) saline ("control") were measured in 10 healthy males in double-blind, randomized fashion. Immediately after each infusion, energy intake at a buffet meal was quantified. Blood glucose rose in response to all glucose infusions (P Ͻ 0.05 vs. control), with the effect of G4 and G2 being greater than that of G1 (P Ͻ 0.05) but with no difference between G2 and G4. The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load (r Ͼ 0.82, P Ͻ 0.05). All glucose infusions suppressed antral (P Ͻ 0.05), but only G4 decreased duodenal, pressure waves (P Ͻ 0.01), resulted in a sustained stimulation of basal pyloric pressure (P Ͻ 0.01), and decreased energy intake (P Ͻ 0.05). In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. These observations have implications for strategies to minimize postprandial glycemic excursions in type 2 diabetes. insulinemia; incretin hormones THE RATE OF GASTRIC EMPTYING of carbohydrate, particularly glucose, has an impact on glycemia (25), appetite (9, 31), and energy intake (32). In healthy subjects, glucose solutions are known to empty from the stomach in an overall linear rate of ϳ2-3 kcal/min (24); this tight regulation results primarily from a length-dependent feedback arising from the small intestine (34), which in turn modulates antropyloroduodenal motility and is associated with the release of a number of gastrointestinal hormones, including cholecystokinin (CCK) (33) and the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) (32,41,51). The relationships of glycemia, hormone release, and changes in gastric motility with the duodenal glucose load, particularly the time course of these effects, are poorly defined.The rate of gastric emptying is a major determinant of the glycemic response to a meal; even relatively minor changes in small intestinal glucose delivery may have major effects on glycemic and insulinemic responses in healthy subjects (7) and non-insulin-treated type 2 diabetics (41). In type 1 diabetes, the initial postprandial insulin requirement is less when gastri...

Background: Dietary interventions represent a promising therapeutic strategy to optimize postprandial glycemia. The addition of protein to oral glucose has been reported to improve the glycemic profile. Objective: The aim of the current study was to evaluate the mechanisms by which protein supplementation lowers the blood glucose response to oral glucose. Design: Nine healthy men were studied on 3 d each in a random order. Subjects consumed 300-mL drinks containing either 50 g glucose (Glucose), 30 g gelatin (Protein), or 50 g glucose with 30 g gelatin (Glucose ѿ Protein) in water labeled with 150 mg [13 C]acetate. Blood and breath samples were subsequently collected for 3 h to measure blood glucose and plasma insulin, glucagon-like peptide 1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) concentrations and gastric half-emptying time, which was calculated from 13 CO 2 excretion. Results: The blood glucose response was less after Glucose ѿ Protein than after Glucose (P 0.005); GIP was lower (P 0.005), and there were no significant differences in plasma insulin or GLP-1. Protein alone stimulated insulin, GLP-1, and GIP (P 0.05 for each) without elevating blood glucose. The gastric half-emptying time was greater after Glucose ѿ Protein than after Glucose (P 0.05) and tended to be greater for Glucose than for Protein (P ҃ 0.06). Conclusions: In healthy humans, the addition of protein to oral glucose lowers postprandial blood glucose concentrations acutely, predominantly by slowing gastric emptying, although protein also stimulates incretin hormones and non-glucose-dependent insulin release.Am J Clin Nutr 2007;86:1364 -8.