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The Journal of Neuroscience, November 10, 2004, 24(45):10260-10265; doi:10.1523/JNEUROSCI.1225-04.2004
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Cellular/Molecular
Bitter Taste Receptors for Saccharin and Acesulfame K
Christina Kuhn,1
Bernd Bufe,1
Marcel Winnig,1
Thomas Hofmann,2
Oliver Frank,2
Maik Behrens,1
Tatjana Lewtschenko,2
Jay P. Slack,3
Cynthia D. Ward,3 and
Wolfgang Meyerhof1
1German Institute of Human Nutrition Potsdam-Rehbruecke, Department of Molecular Genetics, 14558 Nuthetal, Germany, 2Institute of Food Chemistry, University of Münster, 48149 Münster, Germany, and 3Givaudan Flavors Corporation, Cincinnati, Ohio 45216
Weight-conscious subjects and diabetics use the sulfonyl amide sweeteners saccharin and acesulfame K to reduce their calorie and sugar intake. However, the intrinsic bitter aftertaste, which is caused by unknown mechanisms, limits the use of these sweeteners. Here, we show by functional expression experiments in human embryonic kidney cells that saccharin and acesulfame K activate two members of the human TAS2R family (hTAS2R43 and hTAS2R44) at concentrations known to stimulate bitter taste. These receptors are expressed in tongue taste papillae. Moreover, the sweet inhibitor lactisole did not block the responses of cells transfected with TAS2R43 and TAS2R44, whereas it did block the response of cells expressing the sweet taste receptor heteromer hTAS1R2-hTAS1R3. The two receptors were also activated by nanomolar concentrations of aristolochic acid, a purely bitter-tasting compound. Thus, hTAS2R43 and hTAS2R44 function as cognate bitter taste receptors and do not contribute to the sweet taste of saccharin and acesulfame K. Consistent with the in vitro data, cross-adaptation studies in human subjects also support the existence of common receptors for both sulfonyl amide sweeteners.
Key words: TAS2R; bitter taste; saccharin; acesulfame K; aristolochic acid; mRNA localization
Received April 1, 2004;
revised October 1, 2004;
accepted October 5, 2004.
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