Glucagon and its partner insulin are dually linked in both their secretion from islet cells and their action in the liver. Glucagon signaling increases hepatic glucose output, and hyperglucagonemia is partly responsible for the hyperglycemia in diabetes, making glucagon an attractive target for therapeutic intervention. Interrupting glucagon signaling lowers blood glucose but also results in hyperglucagonemia and α-cell hyperplasia. Investigation of the mechanism for α-cell proliferation led to the description of a conserved liver–α-cell axis where glucagon is a critical regulator of amino acid homeostasis. In return, amino acids regulate α-cell function and proliferation. New evidence suggests that dysfunction of the axis in humans may result in the hyperglucagonemia observed in diabetes. This discussion outlines important but often overlooked roles for glucagon that extend beyond glycemia and supports a new role for α-cells as amino acid sensors.

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Alpha 细胞作为氨基酸传感器的主要作用

胰高血糖素及其伴侣胰岛素在它们从胰岛细胞的分泌和它们在肝脏中的作用方面具有双重联系。胰高血糖素信号增加肝葡萄糖输出，高胰高血糖素血症是糖尿病高血糖的部分原因，使胰高血糖素成为治疗干预的有吸引力的目标。中断胰高血糖素信号会降低血糖，但也会导致高胰高血糖素血症和 α 细胞增生。对α细胞增殖机制的研究导致了对保守的肝-α细胞轴的描述，其中胰高血糖素是氨基酸稳态的关键调节剂。作为回报，氨基酸调节α细胞功能和增殖。新的证据表明，人体轴功能障碍可能导致糖尿病中观察到的高胰高血糖素血症。