| UPDATE | 10.02 |
| AUTHOR | Wolfgang Meyerhof of German Institute of Human Nutrition |
| LITERATURE REF. |
Published online: 15 October 2002, doi:10.1038/ng1014 volume 32 no. 3 pp 397 - 401 The human TAS2R16 receptor mediates bitter taste in response to -glucopyranosides Bernd Bufe1, Thomas Hofmann2, Dietmar Krautwurst1, Jan-Dirk Raguse3 & Wolfgang Meyerhof1 Bitter taste generally causes aversion, which protects humans from ingesting toxic substances. But bitter flavors also contribute to the palatability of food and beverages, thereby influencing nutritional habits in humans1. Although many studies have examined bitter taste2-6, the underlying receptor mechanisms remain poorly understood. Anatomical, functional and genetic data from rodents suggest the existence of a family of receptors that are responsive to bitter compounds7-9. Here we report that a human member of this family, TAS2R16, is present in taste receptor cells on the tongue and is activated by bitter -glucopyranosides. Responses to these phytonutrients show a similar concentration dependence and desensitization in transfected cells and in experiments assessing taste perception in humans. Bitter compounds consisting of a hydrophobic residue attached to glucose by a -glycosidic bond activate TAS2R16. Thus, TAS2R16 links the recognition of a specific chemical structure to the perception of bitter taste. If the ability of TAS2R16 to detect substances with common molecular properties is typical of the bitter receptor family, it may explain how a few receptors permit the perception of numerous bitter substances. 1. Department of Molecular Genetics, German Institute of Human Nutrition, Arthur-Scheunert-Allee 114-116, 14558 Potsdam-Rehbrücke, Germany. 2. German Research Center of Food Chemistry, Lichtenbergstrasse 4, Garching, Germany. 3. Clinic and Policlinic for Oral and Maxillofacial Surgery and Plastic Surgery, Charité, Campus Virchow Hospital, Augustenberger Platz 1, Berlin, Germany. Correspondence should be addressed to W Meyerhof. e-mail: meyerhof@mail.dife.de |
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