Pancreatic beta-cell mass and function and therapeutic implications of using antidiabetic medications in type 2 diabetes

Nowadays, the focus of diabetes treatment has switched from lowering the glucose level to preserving glycemic homeostasis and slowing the disease progression. The main pathophysiology of both type 1 diabetes and long-standing type 2 diabetes is pancreatic beta-cell mass loss and dysfunction. According to recent research, human pancreatic beta-cells possess the ability to proliferate in response to elevated insulin demands. It has been demonstrated that in insulin-resistant conditions in humans, such as obesity or pregnancy, the beta-cell mass increases. This ability could be helpful in developing novel treatment approaches to restore a functional beta-cell mass. Treatment strategies aimed at boosting beta-cell function and mass may be a useful tool for managing diabetes mellitus and stopping its progression. This review outlines the processes of beta-cell failure and detail the many beta-cell abnormalities that manifest in people with diabetes mellitus. We also go over standard techniques for determining the mass and function of beta-cells. Lastly, we provide the therapeutic implications of utilizing antidiabetic drugs in controlling the mass and function of pancreatic beta-cells. This review article examines the decline in pancreatic beta-cell mass and function as central to the pathogenesis of type 1 and advanced type 2 diabetes. It discusses the potential for beta-cell regeneration in response to increased insulin demand and evaluates how various antidiabetic medications may affect this process. The therapeutic implications of these findings for the management and treatment of diabetes are explored, offering new insights into potential interventions. image