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Glucagon-Like peptide 1(7-36) Amide Stimulates Exocytosis in Human Pancreatic β-Cells by Both Proximal and Distal Regulatory Steps in Stimulus-Secretion Coupling

机译:胰高血糖素样肽1(7-36)酰胺通过刺激-分泌偶联的近端和远端调节步骤刺激人胰腺β细胞的胞吐作用。

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摘要

The effect of glucagon-like peptide 1 (7-36) amide [GLP-1(7-36) amide] on membrane potential, whole- cell ATP-sensitive potassium channel (K_ATP) and Ca~2+ currents, cytoplasmic Ca~2+ concentration, and exocy- tosis was explored in single human β-cells. GLP-1(7-36) amide induced membrane depolarization that was asso- ciated with inhibition of whole-cell K_ATP current. In addition, GLP-1(7-36) amide (and forskolin) produced greater than fourfold potentiation of Ca~2+-dependent exocytosis. The latter effect resulted in part (40/100) from acceleration of Ca~2+ influx through voltage-depen- dent (L-type) Ca~2+ channels.
机译:胰高血糖素样肽1(7-36)酰胺[GLP-1(7-36)酰胺]对膜电位,全细胞ATP敏感性钾通道(K_ATP)和Ca〜2 +电流,细胞质Ca〜在单个人类β细胞中探索了2+浓度和胞外切作用。 GLP-1(7-36)酰胺诱导的膜去极化作用与抑制全细胞K_ATP电流有关。此外,GLP-1(7-36)酰胺(和福司可林)产生的Ca〜2 +依赖性胞吐作用增强了四倍以上。后一种效应导致部分(40/100)来自通过电压依赖性(L型)Ca〜2 +通道的Ca〜2 +流入加速。

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