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|Title:||Effects of different sweet preloads on incretin hormone secretion, gastric emptying, and postprandial glycemia in healthy humans|
|Citation:||American Journal of Clinical Nutrition, 2012; 95(1):78-83|
|Publisher:||Amer Soc Clinical Nutrition|
|Tongzhi Wu, Beiyi R Zhao, Michelle J Bound, Helen L Checklin, Max Bellon, Tanya J Little, Richard L Young, Karen L Jones, Michael Horowitz, and Christopher K Rayner|
|Abstract:||Background: Macronutrient “preloads” can stimulate glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), slow gastric emptying, and reduce postprandial glycemic excursions. After sweet preloads, these effects may be signaled by sodium-glucose cotransporter-1 (SGLT1), sweet taste receptors, or both. Objective: We determined the effects of 4 sweet preloads on GIP and GLP-1 release, gastric emptying, and postprandial glycemia. Design: Ten healthy subjects were studied on 4 separate occasions each. A preload drink containing 40 g glucose, 40 g tagatose/isomalt mixture (TIM), 40 g 3-O-methylglucose (3OMG; a nonmetabolized substrate of SGLT1), or 60 mg sucralose was consumed 15 min before a 13C-octanoic acid–labeled mashed potato meal. Blood glucose, plasma total GLP-1 and GIP, serum insulin, and gastric emptying were determined. Results: Both glucose and 3OMG stimulated GLP-1 and GIP release in advance of the meal (each P , 0.05), whereas TIM and sucralose did not. The overall postprandial GLP-1 response was greater after glucose, 3OMG, and TIM than after sucralose (P , 0.05), albeit later after TIM than the other preloads. The blood glucose and insulin responses in the first 30 min after the meal were greatest after glucose (each P , 0.05). Gastric emptying was slower after both 3OMG and TIM than after sucralose (each P , 0.05). Conclusions: In healthy humans, SGLT1 substrates stimulate GLP-1 and GIP and slow gastric emptying, regardless of whether they are metabolized, whereas the artificial sweetener sucralose does not. Poorly absorbed sweet tastants (TIM), which probably expose a greater length of gut to nutrients, result in delayed GLP-1 secretion but not in delayed GIP release. These observations have the potential to optimize the use of preloads for glycemic control. This trial was registered at www.actr.org.au as ACTRN12611000775910.|
|Keywords:||Humans; Sugar Alcohols; Gastric Inhibitory Polypeptide; Insulin; Dietary Sucrose; Hexoses; Glucose; Blood Glucose; Disaccharides; Sucrose; Sweetening Agents; Signal Transduction; Gastric Emptying; Postprandial Period; Adult; Female; Male; Sodium-Glucose Transporter 1; Glucagon-Like Peptide 1; Incretins; Young Adult|
|Rights:||© 2012 American Society for Nutrition|
|Appears in Collections:||Medicine publications|
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