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This Article Full Text Full Text (PDF) All Versions of this Article: 296/4/G735    most recent 90708.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ma, J. Articles by Rayner, C. K. Search for Related Content PubMed PubMed Citation Articles by Ma, J. Articles by Rayner, C. K.

HORMONES AND SIGNALING

Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects

Royal Adelaide Hospital, ¹University of Adelaide, Discipline of Medicine, ²Department of Nuclear Medicine, PET and Bone Densitometry, ³Nerve Gut Laboratory, Hanson Institute; ⁴Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, University of Adelaide, Adelaide, Australia

Submitted 18 December 2008 ; accepted in final form 6 February 2009

The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. In mice, sucralose, an artificial sweetener, stimulates GLP-1 release via sweet taste receptors on enteroendocrine cells. We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (300 mosmol/l), all labeled with 150 mg ¹³C-acetate. Blood glucose increased only in response to sucrose (P < 0.05). GLP-1, GIP, and insulin also increased after sucrose (P = 0.0001) but not after either load of sucralose or saline. Gastric emptying of sucrose was slower than that of saline (t₅₀: 87.4 ± 4.1 min vs. 74.7 ± 3.2 min, P < 0.005), whereas there were no differences in t₅₀ between sucralose 0.4 mM (73.7 ± 3.1 min) or 4 mM (76.7 ± 3.1 min) and saline. We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans.