日本群马大学研究人员发现，小鼠的胰腺贝塔细胞中存在的甜味受体能促进胰岛素的分泌，该研究成果有助于开发治疗糖尿病的新方法。
胰腺贝塔细胞对胰岛素的正常分泌发挥着关键作用。过去有部分学者提出胰腺中存在甜味受体，群马大学的研究人员从2008年起对此展开研究。
研究人员在新一期《科学公共图书馆·综合》网络版上发表文章说，他们通过基因比对发现，小鼠贝塔细胞中存在的一种蛋白质和构成舌头的甜味受体的蛋白质的碱基序列完全一样。研究人员用糖精等人造甜味剂刺激贝塔细胞中的这种蛋白质后发现，胰岛素分泌确实得到促进。
本项研究成果表明，如果能很好地刺激胰腺贝塔细胞中的甜味受体，就有可能研发出糖尿病的新疗法。（生物谷Bioon.com）
生物谷推荐原始出处：
PLoS ONE 4(4): e5106. doi:10.1371/journal.pone.0005106
Sweet Taste Receptor Expressed in Pancreatic β-Cells Activates the Calcium and Cyclic AMP Signaling Systems and Stimulates Insulin Secretion
Yuko Nakagawa1, Masahiro Nagasawa1, Satoko Yamada1, Akemi Hara1, Hideo Mogami2, Viacheslav O. Nikolaev3, Martin J. Lohse3, Noriatsu Shigemura4, Yuzo Ninomiya4, Itaru Kojima1*
1 Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan, 2 Department of Physiology, Hamamatsu Medical School, Hamamatsu, Japan, 3 Institute of Pharmacology and Toxicology, University of Wurzburg, Wurzburg, Germany, 4 Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University, Fukuoka, Japan
Background
Sweet taste receptor is expressed in the taste buds and enteroendocrine cells acting as a sugar sensor. We investigated the expression and function of the sweet taste receptor in MIN6 cells and mouse islets.
Methodology/Principal Findings
The expression of the sweet taste receptor was determined by RT–PCR and immunohistochemistry. Changes in cytoplasmic Ca2+ ([Ca2+]c) and cAMP ([cAMP]c) were monitored in MIN6 cells using fura-2 and Epac1-camps. Activation of protein kinase C was monitored by measuring translocation of MARCKS-GFP. Insulin was measured by radioimmunoassay. mRNA for T1R2, T1R3, and gustducin was expressed in MIN6 cells. In these cells, artificial sweeteners such as sucralose, succharin, and acesulfame-K increased insulin secretion and augmented secretion induced by glucose. Sucralose increased biphasic increase in [Ca2+]c. The second sustained phase was blocked by removal of extracellular calcium and addition of nifedipine. An inhibitor of inositol(1, 4, 5)-trisphophate receptor, 2-aminoethoxydiphenyl borate, blocked both phases of [Ca2+]c response. The effect of sucralose on [Ca2+]c was inhibited by gurmarin, an inhibitor of the sweet taste receptor, but not affected by a Gqinhibitor. Sucralose also induced sustained elevation of [cAMP]c, which was only partially inhibited by removal of extracellular calcium and nifedipine. Finally, mouse islets expressed T1R2 and T1R3, and artificial sweeteners stimulated insulin secretion.
