Gut Sensations

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Science  05 Oct 2007:
Vol. 318, Issue 5847, pp. 21
DOI: 10.1126/science.318.5847.21c

Recent studies have helped to define the proteins that transform the arrival of sugars on the tongue into a sensation of sweetness. Two studies suggest that the same pathway functions in the intestinal tract. Jang et al. found that the sugar-sensitive G protein-coupled receptor (T1R2/T1R3) and the G protein subunit gustducin could be detected in enteroendocrine cells—specifically, the L cells, which secrete the appetite-regulating glucagon-like peptide (GLP-1) of the human duodenum. Application of glucose to human L cells resulted in GLP-1 release, which was blocked by an antagonist of T1R3. In mice, gustducin was also present in L cells, and delivering glucose directly into the duodenums (to bypass the tongue) of normal mice and of gustducin-deficient mice showed that GLP-1 secretion was absent in the latter group of animals and that the temporal pattern of insulin secretion was altered. Margolskee et al. connect glucose absorption to glucose sensing via the T1R2/T1R3 pathway. Normal mice, unlike those deficient in gustducin or T1R3, showed an increase in sodium-glucose cotransporter 1 (SGLT1) mRNA and protein and in glucose uptake when fed a high-carbohydrate diet or a low-carb diet containing artificial sweeteners. — NRG

Proc. Natl. Acad. Sci. U.S.A. 104, 15069; 15075 (2007).

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