AMPK and Friends: Central Regulators of β Cell Biology

Abstract

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.

Keywords: AMPK; LKB1; SAD-A; SIK2; diabetes; insulin secretion; pancreatic β cell.