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Sweettaste Receptors and the Secretion of Glucagon-like Peptide-1 and Peptide YY

2014-08-27 03:15:10 | BioPortfolio

Summary

The purpose of this study is to determine the functional significance of sweet taste receptors in the secretion of GI satiety peptides by using a specific sweet taste receptor antagonist to block sweet taste perception in the gut.

Description

There is strong evidence that taste signaling mechanisms identified in the oral epithelium also operate in the gut. It is suggested that open-type enteroendocrine cells directly sense nutrient via alpha-gustducin coupled taste receptors to modulate the secretion of glucagon like peptide-1 (GLP-1) and peptide YY (PYY). Several nutrient responsive G-protein coupled receptors have been identified in the human gut, including the sweet taste responsive T1R2/T1R3 heterodimer, the amino acid/umami responsive T1R1/T1R3 as well as GPR120 for unsaturated long-chain free fatty acids.The functional significance of sweet taste receptors in glucose stimulated secretion of GLP-1 and PYY will be determined by intragastric infusion of 75 g glucose with or without different concentrations of lactisole, a sweet taste receptor antagonist (150, 300, 450 ppm) in a double blind, 4 way crossover trial including 16 healthy subjects (4 male, 4 female).

Study Design

Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Pharmacodynamics Study, Intervention Model: Crossover Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Basic Science

Conditions

Gastrointestinal Satiety Peptides

Intervention

lactisole

Location

University Hospital Basel, Clinical Research Center
Basel
Switzerland
4031

Status

Completed

Source

University Hospital, Basel, Switzerland

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:15:10-0400

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Medical and Biotech [MESH] Definitions

A peptide, of about 33 amino acids, secreted by the upper INTESTINAL MUCOSA and also found in the central nervous system. It causes gallbladder contraction, release of pancreatic exocrine (or digestive) enzymes, and affects other gastrointestinal functions. Cholecystokinin may be the mediator of satiety.

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