beta-cell function and anti-diabetic pharmacotherapy

Abstract

Type 2 diabetes is a chronic disease characterized by progressive worsening of glycaemic control as indicated by the United Kingdom Prospective Diabetes Study (UKPDS). The progressive nature of the disease is mainly due to continuous loss of beta-cell mass and function. Though much of this loss is due to intrinsic defects of the beta-cell several factors may accelerate such process. These include the metabolic environment where hyperglycaemia and increased circulating free-fatty acid exert a toxic effect on the beta-cell. Therefore, tight metabolic control may prevent not only the risk of long-term diabetic complication but also preserve beta-cell function. Several therapeutic agents are currently used for treatment of type 2 diabetic patients. However, their effect on maintenance of beta-cell function has not been yet systematically reviewed. By literature searching we have then analysed in detail the effect of sulfonylureas and non-sulfonylureic secretagogues, incretin-mimetics, insulin sensitizers, alpha-glucosidase inhibitors, and insulin on beta-cell function. Moreover, promising future approaches aiming at preserving beta-cell function and mass are discussed.