Artificial Sweeteners Have No Effect on Gastric Emptying, Glucagon-Like Peptide-1, or Glycemia After Oral Glucose in Healthy Humans

  1. Christopher K. Rayner, MBBS, PHD1,2
  1. 1Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, Australia
  2. 2Centre of Research Excellence in Translating Nutritional Science to Good Health, University of Adelaide, Adelaide, Australia
  3. 3Department of Nuclear Medicine, Royal Adelaide Hospital, Adelaide, Australia
  4. 4Nerve-Gut Research Laboratory, Royal Adelaide Hospital, Adelaide, Australia
  1. Corresponding author: Christopher K. Rayner, chris.rayner{at}adelaide.edu.au.

Intestinal exposure to glucose stimulates the release of glucagon-like peptide-1 (GLP-1), slows subsequent gastric emptying, and reduces appetite. These responses are signaled, at least in part, by intestinal “sweet taste receptors” (STRs), including taste receptor type 1 members 2 and 3 (T1R2, T1R3), and their cellular signaling partners α-gustducin and transient receptor potential cation channel subfamily M member 5 (TRPM5) (1). A recent study by Brown et al. (2) in healthy humans reported that oral ingestion of “diet soda,” containing both sucralose (46 mg) and acesulfame potassium (AceK) (26 mg), augmented GLP-1 release by more than one-third after an oral glucose load given 10 min later compared with carbonated water, suggesting a potential synergy between artificial sweeteners and glucose in stimulating GLP-1 secretion. The design of that study was, however, suboptimal, as the diet soda contained a number of substances (including caramel color, gum acacia, natural flavors, citric acid, potassium benzoate, phosphoric acid, and potassium citrate) that were not controlled for. Therefore, we evaluated whether oral administration of sucralose and AceK in doses comparable with those used by Brown et al. (2) would augment the GLP-1 response to oral glucose and modulate gastric emptying or glycemia …

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