Jing Ma, Jessica Chang, Helen L Checklin, Richard L Young, Karen L Jones, Michael Horowitz, Christopher K Rayner
Journal: The British journal of nutrition 2010;104(6):803-6
PMID: 20420761
Recent animal-based studies have shown that the artificial sweetener, sucralose, stimulates glucose absorption by enhancing apical availability of the transporter GLUT2 [is a transmembrane carrier protein that enables protein facilitated glucose movement across cell membranes]. The aim of this study was to evaluate whether exposure of the proximal small intestine to sucralose affects the subsequent response to glucose in terms of the rate of glucose absorption and the glycaemic response. This study is a randomised, single-blind, cross-over design study for which ten healthy subjects (eight males and two females) were enrolled and studied twice. Results indicate that: - there was no difference in baseline glucose concentrations between the two study days. - there was no difference in baseline glucagon-like peptide-1 [a hormone produced in the gut and released in response to food] concentrations between the two study days. - intraduodenal administration of sucralose has no effect on the rate of glucose absorption from the lumen of the small intestine. Authors conclude that acute intraduodenal administration of sucralose does not enhance the absorption of glucose from the small intestine or increase blood glucose or plasma glucagon-like peptide-1 concentrations in healthy human subjects.
It has been reported that the artificial sweetener, sucralose, stimulates glucose absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects glucose absorption and/or the glycaemic response to an intraduodenal (ID) glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0.9% saline) or control (0.9% saline) at 4 ml/min for 150 min (T = - 30 to 120 min). After 30 min (T = 0), glucose (25 %) and its non-metabolised analogue, 3-O-methylglucose (3-OMG; 2.5 %), were co-infused intraduodenally (T = 0-120 min; 4.2 kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood glucose, plasma glucagon-like peptide-1 (GLP-1) and serum 3-OMG concentrations increased during ID glucose/3-OMG infusion (P < 0.005 for each). However, there were no differences in blood glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of glucose absorption or the glycaemic or incretin response to ID glucose infusion when given acutely in healthy human subjects.
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