Sener A, Malaisse W J
Nature. 1980 Nov 13;288(5787):187-9. doi: 10.1038/288187a0.
The release of insulin evoked by nutrients in the pancreatic beta-cell is attributed to either the activation of a stereospecific receptor by the nutrient molecule itself or the generation of one or more signal(s) through the intracellular metabolism of the nutrient secretagogue. The first of these hypotheses is apparently supported by the fact the nonmetabolized amino acids, especially the L-leucine analogue b(-)2-amino-bicyclo[2,2,1]heptane-2-carbocyclic acid (BCH), stimulate insulin release. However, we now report evidence in support of the second hypothesis. We present data consistent with the idea that BCH induces insulin release through the allosteric activation of glutamate dehydrogenase. This is compatible with the fuel hypothesis, which states that the secretory response to nutrient secretagogues depends always on an increase of catabolic fluxes in the islet cells.
胰腺β细胞中营养物质引发的胰岛素释放，要么归因于营养分子自身对立体特异性受体的激活，要么归因于通过营养促分泌剂的细胞内代谢产生一种或多种信号。这些假说中的第一个显然得到了以下事实的支持：非代谢氨基酸，尤其是L-亮氨酸类似物b(-)2-氨基-双环[2,2,1]庚烷-2-碳环酸（BCH），能刺激胰岛素释放。然而，我们现在报告支持第二个假说的证据。我们提供的数据与以下观点一致：BCH通过谷氨酸脱氢酶的变构激活诱导胰岛素释放。这与燃料假说相符，该假说认为对营养促分泌剂的分泌反应总是取决于胰岛细胞中分解代谢通量的增加。
