Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 38, Pages 15069-15074Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0706890104
Keywords
enteroendocrine cells; gastrointestinal chemosensation; glucose sensor; incretin
Categories
Funding
- Intramural NIH HHS Funding Source: Medline
- NIDCD NIH HHS [R01 DC003155, DC003155, DC007399, DC003055, R01 DC003055, R21 DC007399] Funding Source: Medline
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Glucagon-like peptide-1 (GLP-1), released from gut endocrine L cells in response to glucose, regulates appetite, insulin secretion, and gut motility. How glucose given orally, but not systemically, induces GILP-1 secretion is unknown. We show that human duodenal L cells express sweet taste receptors, the taste G protein gustducin, and several other taste transduction elements. Mouse intestinal L cells also express a-gustducin. Ingestion of glucose by alpha-gustducin null mice revealed deficiencies in secretion of GLP-1 and the regulation of plasma insulin and glucose. Isolated small bowel and intestinal villi from alpha-gustducin null mice showed markedly defective GILP-1 secretion in response to glucose. The human L cell line NCI-H716 expresses a-gustducin, taste receptors, and several other taste signaling elements. GLP-1 release from NCI-H716 cells was promoted by sugars and the noncaloric sweetener sucralose, and blocked by the sweet receptor antagonist lactisole or siRNA for a-gustducin. We conclude that L cells of the gut taste glucose through the same mechanisms used by taste cells of the tongue. Modulating GLP-1 secretion in gut taste cells may provide an important treatment for obesity, diabetes and abnormal gut motility.
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