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Am J Physiol Endocrinol Metab (December 23, 2008). doi:10.1152/ajpendo.90636.2008
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Submitted on July 28, 2008
Revised on December 16, 2008
Accepted on December 16, 2008

Incretin Release from Gut is Acutely Enhanced by Sugar but Not by Sweeteners In Vivo

Yukihiro Fujita1, Rhonda D. Wideman2, Madeleine Speck2, Ali Asadi2, David S King2, Travis D. Webber2, Masakazu Haneda3, and Timothy J Kieffer2*

1 Asahikawa Medical College
2 University of British Columbia
3 Shiga University of Medical Science

* To whom correspondence should be addressed. E-mail: tim.kieffer{at}ubc.ca.

Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are released during meals from endocrine cells located in the gut mucosa and stimulate insulin secretion from pancreatic {beta}-cells in a glucose-dependent manner. Although the gut epithelium senses luminal sugars, the mechanism of sugar sensing and its downstream events coupled to the release of the incretin hormones are not clearly elucidated. Recently it was reported that sucralose, a sweetener that activates sweet receptors of taste buds, triggers incretin release from a murine enteroendocrine cell line in vitro. We confirmed that immunoreactivity of {alpha}-gustducin, a key G-coupled protein involved in taste sensing, is co-localized with GIP in rat duodenum. We investigated whether secretion of incretins in response to carbohydrates is mediated via taste receptors by feeding rats the sweet tasting compounds saccharin, acesulfame potassium, D-tryptophan, sucralose, or stevia. Oral gavage of these sweeteners did not reduce the blood glucose excursion to a subsequent intraperitoneal glucose tolerance test. Neither oral sucralose nor oral stevia reduced blood glucose levels in Zucker diabetic fatty rats. Finally, whereas oral glucose increased plasma GIP levels ~4-fold and GLP-1 levels ~2.5-fold post administration, none of the sweeteners tested significantly increased levels of these incretins. Collectively, our findings do not support the concept that release of incretins from enteroendocrine cells is triggered by carbohydrates via a pathway identical to the sensation of 'sweet taste' in the tongue.




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