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首页> 外文期刊>FEBS Open Bio >Sucralose activates an ERK1/2–ribosomal protein S6 signaling axis
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Sucralose activates an ERK1/2–ribosomal protein S6 signaling axis

机译:三氯蔗糖激活ERK1 / 2–核糖体蛋白S6信号轴

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The sweetener sucralose can signal through its GPCR receptor to induce insulin secretion from pancreatic β cells, but the downstream signaling pathways involved are not well‐understood. Here we measure responses to sucralose, glucagon‐like peptide 1, and amino acids in MIN6 β cells. Our data suggest a signaling axis, whereby sucralose induces calcium and cAMP, activation of ERK1/2, and site‐specific phosphorylation of ribosomal protein S6. Interestingly, sucralose acted independently of mTORC1 or ribosomal S6 kinase (RSK). These results suggest that sweeteners like sucralose can influence β‐cell responses to secretagogues like glucose through metabolic as well as GPCR‐mediated pathways. Future investigation of novel sweet taste receptor signaling pathways in β cells will have implications for diabetes and other emergent fields involving these receptors.
机译:甜味剂三氯蔗糖可以通过其GPCR受体发出信号,以诱导胰腺β细胞分泌胰岛素,但所涉及的下游信号通路尚不为人所知。在这里,我们测量了MIN6β细胞中对三氯蔗糖,胰高血糖素样肽1和氨基酸的反应。我们的数据提示了一个信号轴,三氯蔗糖由此诱导了钙和cAMP,ERK1 / 2的激活以及核糖体蛋白S6的位点特异性磷酸化。有趣的是,三氯蔗糖的作用独立于mTORC1或核糖体S6激酶(RSK)。这些结果表明,甜味剂(如三氯蔗糖)可以通过代谢以及GPCR介导的途径影响β细胞对促分泌素(如葡萄糖)的反应。 β细胞中新型甜味受体信号传导途径的未来研究将对糖尿病和涉及这些受体的其他新兴领域产生影响。

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