If left unchecked, prediabetic hyperglycemia can progress to diabetes and often life-threatening attendant secondary complications. Central to the process of glucose homeostasis are pancreatic β cells, which sense elevations in plasma glucose and additional dietary components and respond by releasing the appropriate quantity of insulin, ensuring the arrest of hepatic glucose output and glucose uptake in peripheral tissues. Given that β cell failure is associated with the transition from prediabetes to diabetes, improved β cell function ('compensation') has a central role in preventing type 2 diabetes mellitus (T2DM). Recent data have shown that both insulin secretion and β cell mass dynamics are regulated by the liver kinase B1-AMP-activated kinase (LKB1-AMPK) pathway and related kinases of the AMPK family; thus, an improved understanding of the biological roles of AMPK in the β cell is now of considerable interest.

中文翻译：

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AMPK 和朋友：β 细胞生物学的中枢调节剂

如果不加以控制，糖尿病前期的高血糖症可能会发展为糖尿病，并且通常会危及生命的继发性并发症。葡萄糖稳态过程的核心是胰腺 β 细胞，它感知血浆葡萄糖和其他饮食成分的升高，并通过释放适量的胰岛素做出反应，确保肝葡萄糖输出和外周组织葡萄糖摄取的停滞。鉴于 β 细胞衰竭与从前驱糖尿病到糖尿病的转变有关，改善 β 细胞功能（“代偿”）在预防 2 型糖尿病 (T2DM) 中起着核心作用。最近的数据表明，胰岛素分泌和 β 细胞质量动态均受肝激酶 B1-AMP 活化激酶 (LKB1-AMPK) 通路和 AMPK 家族相关激酶的调节；因此，