肾上腺素和去甲肾上腺素抑制胰岛素分泌
中文名称
通路描述
肾上腺素（肾上腺素）和去甲肾上腺素（去甲肾上腺素）抑制胰岛β细胞中的胰岛素分泌。在细胞中观察到四个效应：1. 抑制分泌颗粒的胞吐作用（主要效应）；2. 打开ATP敏感的钾通道（KATP通道）并复极化细胞；3. 关闭L型电压依赖性钙通道并抑制钙内流；4. 抑制腺苷酸环化酶活性。在β细胞中，肾上腺素/去甲肾上腺素信号的第一步是肾上腺素或去甲肾上腺素与α2肾上腺素能受体结合，这是一种G蛋白偶联受体。结合激活了异三聚体Gi和Go复合物中的α亚基，使其交换GDP为GTP，形成活性Gα:GTP复合物。使用针对小鼠α亚基的特异性抗体实验表明，Giα-1、Giα-2和Goα-2负责肾上腺素效应。异三聚体G蛋白的β和γ亚基的确切身份尚不清楚。
英文描述
Adrenaline,noradrenaline inhibits insulin secretion The catecholamines adrenaline (epinephrine) and noradrenaline (norepinephrine) inhibit insulin secretion from pancreatic beta cells. Four effects are seen in the cells:
1. Inhibition of exocytosis of secretory granules, the major effect.
2. Opening of ATP-sensitive potassium channels (KATP channels) and repolarization of the cell.
3. Closing of L-type voltage-dependent calcium channels and inhibition of calcium influx.
4. Inhibition of adenylyl cyclase activity.
The first event in adrenaline/noradrenaline signaling in beta cells is the binding of adrenaline or noradrenaline to alpha-2 adrenergic receptors, which are G-protein coupled receptors. Binding activates the alpha subunits in heterotrimeric Gi and Go complexes to exchange GDP for GTP, forming the active G alpha:GTP complex. Experiments using specific antibodies against the alpha subunits in mice show that Gi alpha-1, Gi alpha-2, and Go alpha-2 are responsible for adrenergic effects. The exact beta and gamma subunits of the heterotrimeric G-proteins are unknown.
After activation by GTP, the heterotrimeric complex dissociates into the G alpha:GTP complex and the beta:gamma complex. The G alpha:GTP complex causes the inhibition of exocytosis by an unknown mechanism that involves protein acylation. This is responsible for most of the observed inhibition of insulin secretion. Additionally, the G alpha:GTP complex activates (opens) KATP channels, allowing the cell to repolarize. The beta:gamma complex inhibits (closes) voltage-dependent calcium channels, reducing the intracellular calcium concentration, and inhibits adenylyl cyclase, reducing the intracellular cAMP concentration.
1. Inhibition of exocytosis of secretory granules, the major effect.
2. Opening of ATP-sensitive potassium channels (KATP channels) and repolarization of the cell.
3. Closing of L-type voltage-dependent calcium channels and inhibition of calcium influx.
4. Inhibition of adenylyl cyclase activity.
The first event in adrenaline/noradrenaline signaling in beta cells is the binding of adrenaline or noradrenaline to alpha-2 adrenergic receptors, which are G-protein coupled receptors. Binding activates the alpha subunits in heterotrimeric Gi and Go complexes to exchange GDP for GTP, forming the active G alpha:GTP complex. Experiments using specific antibodies against the alpha subunits in mice show that Gi alpha-1, Gi alpha-2, and Go alpha-2 are responsible for adrenergic effects. The exact beta and gamma subunits of the heterotrimeric G-proteins are unknown.
After activation by GTP, the heterotrimeric complex dissociates into the G alpha:GTP complex and the beta:gamma complex. The G alpha:GTP complex causes the inhibition of exocytosis by an unknown mechanism that involves protein acylation. This is responsible for most of the observed inhibition of insulin secretion. Additionally, the G alpha:GTP complex activates (opens) KATP channels, allowing the cell to repolarize. The beta:gamma complex inhibits (closes) voltage-dependent calcium channels, reducing the intracellular calcium concentration, and inhibits adenylyl cyclase, reducing the intracellular cAMP concentration.
所含基因
28 个基因