Diabetes is both a metabolic and an immune disorder. One intriguing link between the two is the serine-threonine protein kinase mammalian target of rapamycin (mTOR). As a component of the PI3K/Akt pathway and other cellular signals, mTOR is a key regulator of fuel metabolism and function of both pancreatic islet β cells and immune cells. Consequently, it seems that mTOR has both anti- and prodiabetic effects. On the one hand, activation of mTOR in β cells can increase their growth and proliferation, opposing impairments of insulin secretion in diabetes. On the other, activation of mTOR signaling in specific immune cells alters their fuel metabolism, amplifying their contributions to β-cell dysfunction, contributing to the development of diabetes. In this review, we focus on roles of mTOR signaling in pancreatic β cells and immune cells and their implications in the pathogenesis and treatment of diabetes.
Keywords: immune cells; inflammation; insulin resistance; islet β-cell proliferation; metabolism.
©2018 Society for Leukocyte Biology.