The physiological effects of glucagon-like peptide-1 (GLP-1) are of immense interest because of the potential clinical relevance of this peptide. Produced in intestinal L-cells through posttranslational processing of the proglucagon gene, GLP-1 is released from the gut in response to nutrient ingestion. Peripherally, GLP-1 is known to affect gut motility, inhibit gastric acid secretion, and inhibit glucagon secretion. In the central nervous system, GLP-1 induces satiety, leading to reduced weight gain. In the pancreas, GLP-1 is now known to induce expansion of insulin-secreting beta-cell mass, in addition to its most well-characterized effect: the augmentation of glucose-stimulated insulin secretion. GLP-1 is believed to enhance insulin secretion through mechanisms involving the regulation of ion channels (including ATP-sensitive K(+) channels, voltage-dependent Ca(2+) channels, voltage-dependent K(+) channels, and nonselective cation channels) and by the regulation of intracellular energy homeostasis and exocytosis. The present article will focus principally on the mechanisms proposed to underlie the glucose dependence of GLP-1's insulinotropic effect.

中文翻译：

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GLP-1在葡萄糖刺激胰岛素分泌过程中的多重作用

由于该肽的潜在临床相关性，胰高血糖素样肽-1 (GLP-1) 的生理作用引起了极大的兴趣。GLP-1 通过胰高血糖素原基因的翻译后加工在肠道 L 细胞中产生，响应营养摄入从肠道释放。在外周，已知 GLP-1 会影响肠道运动、抑制胃酸分泌和抑制胰高血糖素分泌。在中枢神经系统中，GLP-1 会引起饱腹感，从而减少体重增加。在胰腺中，现在已知 GLP-1 可诱导分泌胰岛素的 β 细胞群的扩张，此外还有其最明显的作用：增加葡萄糖刺激的胰岛素分泌。GLP-1 被认为通过涉及调节离子通道（包括 ATP 敏感 K(+) 通道、电压依赖性 Ca(2+) 通道、电压依赖性 K(+) 通道和非选择性阳离子通道）以及细胞内能量稳态和胞吐作用的调节。本文将主要关注 GLP-1 促胰岛素作用的葡萄糖依赖性所提出的机制。