日本群馬大學(xué)研究人員發(fā)現(xiàn),，小鼠的胰腺貝塔細(xì)胞中存在的甜味受體能促進(jìn)胰島素的分泌，該研究成果有助于開(kāi)發(fā)治療糖尿病的新方法,。
胰腺貝塔細(xì)胞對(duì)胰島素的正常分泌發(fā)揮著關(guān)鍵作用。過(guò)去有部分學(xué)者提出胰腺中存在甜味受體,，群馬大學(xué)的研究人員從2008年起對(duì)此展開(kāi)研究,。
研究人員在新一期《科學(xué)公共圖書(shū)館·綜合》網(wǎng)絡(luò)版上發(fā)表文章說(shuō)，他們通過(guò)基因比對(duì)發(fā)現(xiàn),，小鼠貝塔細(xì)胞中存在的一種蛋白質(zhì)和構(gòu)成舌頭的甜味受體的蛋白質(zhì)的堿基序列完全一樣,。研究人員用糖精等人造甜味劑刺激貝塔細(xì)胞中的這種蛋白質(zhì)后發(fā)現(xiàn)，胰島素分泌確實(shí)得到促進(jìn),。
本項(xiàng)研究成果表明,，如果能很好地刺激胰腺貝塔細(xì)胞中的甜味受體，就有可能研發(fā)出糖尿病的新療法,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
