β-cell preservation: a potential role for thiazolidinediones to improve clinical care in Type 2 diabetes

Type 2 diabetes is caused by progressively increasing insulin resistance coupled with deteriorating β‐cell function, and there is a growing body of evidence to suggest that both of these defects precede hyperglycaemia by many years. Several studies have demonstrated the importance of maintaining β‐cell function in patients with Type 2 diabetes. This review explores parameters used to indicate β‐cell dysfunction, in Type 2 diabetes and in individuals with a predisposition to the disease. A genetic element undoubtedly underlies β‐cell dysfunction; however, a number of modifiable components are also associated with β‐cell deterioration, such as chronic hyperglycaemia and elevated free fatty acids. There is also evidence for a link between pro‐inflammatory cytokines and impairment of insulin‐signalling pathways in the β‐cell, and the potential role of islet amyloid deposition in β‐cell deterioration continues to be a subject for debate. The thiazolidinediones are a class of agents that have demonstrated clinical improvements in indices of β‐cell dysfunction and have the potential to improve β‐cell function. Data are accumulating to show that this therapeutic group offers a number of advantages over traditionally employed oral agents, and these data demonstrate the growing importance of thiazolidinediones in Type 2 diabetes management.