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首页> 外文期刊>Cell metabolism >GLP-1 inhibits and adrenaline stimulates glucagon release by differential modulation of N- and L-type Ca2+ channel-dependent exocytosis.
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GLP-1 inhibits and adrenaline stimulates glucagon release by differential modulation of N- and L-type Ca2+ channel-dependent exocytosis.

机译：GLP-1通过差异调节N型和L型Ca2 +通道依赖性胞吐作用来抑制和刺激肾上腺素释放。

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摘要

Glucagon secretion is inhibited by glucagon-like peptide-1 (GLP-1) and stimulated by adrenaline. These opposing effects on glucagon secretion are mimicked by low (1-10 nM) and high (10 muM) concentrations of forskolin, respectively. The expression of GLP-1 receptors in alpha cells is <0.2% of that in beta cells. The GLP-1-induced suppression of glucagon secretion is PKA dependent, is glucose independent, and does not involve paracrine effects mediated by insulin or somatostatin. GLP-1 is without much effect on alpha cell electrical activity but selectively inhibits N-type Ca(2+) channels and exocytosis. Adrenaline stimulates alpha cell electrical activity, increases [Ca(2+)](i), enhances L-type Ca(2+) channel activity, and accelerates exocytosis. The stimulatory effect is partially PKA independent and reduced in Epac2-deficient islets. We propose that GLP-1 inhibits glucagon secretion by PKA-dependent inhibition of the N-type Ca(2+) channels via a small increase in intracellular cAMP ([cAMP](i)). Adrenaline stimulates L-type Ca(2+) channel-dependent exocytosis by activation of the low-affinity cAMP sensor Epac2 via a large increase in [cAMP](i).
机译：胰高血糖素样肽-1（GLP-1）抑制胰高血糖素的分泌，并被肾上腺素刺激。低浓度（1-10 nM）和高浓度（10μM）的毛喉素可模拟这些对胰高血糖素分泌的相反作用。 GLP-1受体在α细胞中的表达小于β细胞中0.2％的表达。 GLP-1诱导的胰高血糖素分泌抑制是PKA依赖性的，与葡萄糖无关，并且不涉及胰岛素或生长抑素介导的旁分泌作用。 GLP-1对alpha细胞的电活动没有太大影响，但选择性地抑制N型Ca（2+）通道和胞吐作用。肾上腺素刺激α细胞电活动，增加[Ca（2 +）]（i），增强L型Ca（2+）通道活性，并加速胞吐作用。刺激作用部分不依赖PKA，在Epac2缺失的胰岛中降低。我们建议，GLP-1通过细胞内cAMP（[cAMP]（i））的少量增加，通过PKA依赖性的N型Ca（2+）通道抑制胰高血糖素分泌。肾上腺素通过[cAMP]（i）的大幅增加激活低亲和力cAMP传感器Epac2来刺激L型Ca（2+）通道依赖性胞吐作用。

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