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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion
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Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion

机译:β细胞中的甜味受体信号转导果糖诱导的葡萄糖刺激的胰岛素分泌增强

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摘要

The increase in circulating glucose levels that occurs after a meal is the primary stimulus of insulin release from beta cells (i.e., endocrine cells residing in the pancreatic islets of Langerhans). In turn, circulating insulin facilitates glucose clearance, restoring levels of glucose in the blood to premeal levels and preventing further insulin secretion. Although glucose is indispensable for this insulin release, numerous other molecules, including the major dietary sugar fructose, can help stimulate insulin secretion in vitro (1). Here, we describe a pathway for the regulation of postmeal insulin release in which fructose leads to improved glucose-stimulated insulin secretion mediated by sweet taste receptors on the surface of beta cells.
机译:饭后循环葡萄糖水平的增加是胰岛素从β细胞(即,位于Langerhans胰岛的内分泌细胞)释放的主要刺激。反过来,循环胰岛素有助于清除葡萄糖,将血液中的葡萄糖水平恢复到餐前水平,并防止进一步的胰岛素分泌。尽管葡萄糖对于这种胰岛素释放是必不可少的,但许多其他分子,包括主要的饮食糖果糖,也可以帮助刺激体外胰岛素的分泌(1)。在这里,我们描述了一种调节餐后胰岛素释放的途径,其中果糖导致β细胞表面甜味受体介导的葡萄糖刺激的胰岛素分泌的改善。

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    Metabolic Signaling and Disease, Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827;

    Metabolic Signaling and Disease, Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827;

    Metabolic Signaling and Disease, Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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  • 正文语种 eng
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