The double-edged effect of autophagy in pancreatic beta cells and diabetes

Abstract

Autophagy is an intracellular catabolic system, which enables cells to capture cytoplasmic components for degradation within lysosomes. Autophagy is involved in development, differentiation and tissue remodeling in various organisms, and is also implicated in certain diseases. Recent studies demonstrate that autophagy is necessary to maintain architecture and function of pancreatic beta cells. Altered autophagy is also involved in pancreatic beta cell death. Whether autophagy plays a protective or harmful role in diabetes is still not clear. In this review, we will summarize the current knowledge about the role of autophagy in pancreatic beta cell and diabetes.

Figure 1

Autophagy, apoptosis and diabetes. ER and oxidative stress triggered by hyperglycemia or hyperlipaemia induce autophagy in pancreatic beta cells. Phosphatidylinositol 3-kinase (PI3K) iii, expression of Atg7, Atg5, Beclin 1 and LAMP-2 play a crucial role in regulating autophagy. Whether autophagy plays a protective or harmful role in diabetes is still not clear, and many questions need to be answered. For instance, does autophagy-dependent apoptosis occur in pancreatic beta cells? Is there a cross-talk between autophagy and apoptosis in the beta cell through cleavage products of Beclin 1 and Atg5, as demonstrated in other cellular systems? These and other questions await the results of further research.