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Taste Cells of the Gut and Gastrointestinal Chemosensation

¹ National Institute on Aging/National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224;
² Department of Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029

SUMMARY

Taste receptors, the taste G-protein gustducin, and downstream signaling elements known to underlie the detection and transduction of bitter, sweet, and umami (monosodium glutamate–containing) compounds in taste buds of the tongue are present also in specific endocrine cells of the gut: the enteroendocrine K and L cells. Glucose in the gut activates sweet taste receptors and gustducin present in the intestine’s enteroendocrine L cells, leading to secretion of glucagon-like peptide-1 (GLP-1) from these cells. GLP-1 and glucose-dependent insulinotropic peptide (GIP) are incretin hormones, which augment insulin release from the beta cells of the pancreas. GLP-1, GIP, and other gut hormones released from the K and L cells affect insulin secretion, glucose homeostasis, nutrient absorption and other gut functions. Glucose transport into enterocytes via Na+,glucose cotransporter 1 (SGLT1) and GLUT2 appears to be regulated by the gustducin- and sweet receptor-expressing enteroendocrine cells. In response to sugar ingestion, knockout mice lacking gustducin show deficits in the release of GLP-1 and insulin, in glucose homeostasis, and in upregulation of SGLT1. Apparently, the gut "tastes" sugars and sweeteners in much the same way as does the tongue and by using many of the same signaling elements. Taste receptors and other taste signaling elements in gut may be contributors to obesity, diabetes, metabolic syndrome and other diet-related disorders. Gut-expressed taste elements are attractive targets for therapeutic intervention.