Diabetes

Mitochondrial metabolism and dynamics in pancreatic beta cell glucose sensing

Healthy mitochondria play a vital role in insulin secretion, particularly in pancreatic islet cells. Glucose stimulates mitochondrial oxidative metabolism in these cells, which is essential for normal insulin release. Additionally, incretins like GLP1 enhance the effects of glucose on mitochondrial function, further supporting insulin secretion. However, when mitochondria become fragmented due to decreased levels of mitofusin, as seen in conditions like diabetes, they become dysfunctional. This leads to inadequate maintenance of mitochondrial DNA content and respiratory chain function. As a result, insulin secretion is impaired.

Unhealthy mitochondria with altered structure and function negatively impact insulin secretion. The disrupted mitochondrial integrity compromises the normal calcium dynamics, beta-cell connectivity, and insulin secretion that rely on proper mitochondrial function. This dysfunction can be detrimental in diabetes, where maintaining optimal glucose regulation is crucial. Changes in mitochondrial metabolism-related genes have been observed in both type 1 and type 2 diabetes. Strategies that promote mitochondrial health may hold therapeutic potential.

Mitochondrial function is also important in regulating the secretion of other hormones in pancreatic islet cells, such as glucagon and somatostatin, which represents an emerging area of interest.