Multimodal function of the sweet taste receptor expressed in pancreatic β-cells: generation of diverse patterns of intracellular signals by sweet agonists

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Author(s)

    • Nakagawa Yuko
    • Institute for Molecular & Cellular Regulation, Gunma University, Maebashi 371-8512, Japan
    • Nagasawa Masahiro
    • Institute for Molecular & Cellular Regulation, Gunma University, Maebashi 371-8512, Japan
    • Mogami Hideo
    • Faculty of Health and Medical Science, Tokoha University, Hamamatsu 420-0911, Japan
    • Lohse Martin
    • Institute of Pharmacology and Toxicology, University of Wurzburg, Wurzburg 97070, Germany
    • Ninomiya Yuzo
    • Graduate School of Dental Science, Kyushu University, Fukuoka 812-8582, Japan
    • Kojima Itaru
    • Institute for Molecular & Cellular Regulation, Gunma University, Maebashi 371-8512, Japan

Abstract

The sweet taste receptor is expressed in the taste bud and is activated by numerous sweet molecules with diverse chemical structures. It is, however, not known whether these sweet agonists induce a similar cellular response in target cells. Using MIN6 cells, a pancreatic β-cell line expressing endogenous sweet taste receptor, we addressed this question by monitoring changes in cytoplasmic Ca<sup>2+</sup> ([Ca<sup>2+</sup>]<sub>i</sub>) and cAMP ([cAMP]<sub>i</sub>) induced by four sweet taste receptor agonists. Glycyrrhizin evoked sustained elevation of [Ca<sup>2+</sup>]<sub>i</sub> but [cAMP]<sub>i</sub> was not affected. Conversely, an artificial sweetener saccharin induced sustained elevation of [cAMP]<sub>i</sub> but did not increase [Ca<sup>2+</sup>]<sub>i</sub>. In contrast, sucralose and acesulfame K induced rapid and sustained increases in both [Ca<sup>2+</sup>]<sub>i</sub> and [cAMP]<sub>i</sub>. Although the latter two sweeteners increased [Ca<sup>2+</sup>]<sub>i</sub> and [cAMP]<sub>i</sub>, their actions were not identical: [Ca<sup>2+</sup>]<sub>i</sub> response to sucralose but not acesulfame K was inhibited by gurmarin, an antagonist of the sweet taste receptor which blocks the gustducin-dependent pathway. In addition, [Ca<sup>2+</sup>]<sub>i</sub> response to acesulfame K but not to sucralose was resistant to a G<sub>q</sub> inhibitor. These results indicate that four types of sweeteners activate the sweet taste receptor differently and generate distinct patterns of intracellular signals. The sweet taste receptor has amazing multimodal functions producing multiple patterns of intracellular signals.

Journal

  • Endocrine Journal

    Endocrine Journal 60(10), 1191-1206, 2013

    The Japan Endocrine Society

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