In addition to its central role in the development of microvascular complications, hyperglycaemia plays an important role in the pathogenesis of type 2 diabetes, i.e. glucotoxicity. Thus, effective glycaemic control not only reduces the incidence of microvascular complications, but also corrects the metabolic abnormalities that contribute to the progression of the disease. Progressive beta-cell failure and side effects associated with therapy, such as hypoglycaemia and weight gain, present obstacles to the achievement of optimal durable glycaemic control in subjects with type 2 diabetes. Most recently, inhibitors of the renal sodium glucose co-transporter have been developed to produce glucosuria and reduce the plasma glucose concentration. Because the mechanism of action of these oral antidiabetic agents is independent of beta-cell and tissue sensitivity to insulin, they improve glycaemic control while avoiding hypoglycaemia and promoting weight loss. In this article, we will summarise the available data concerning the mechanism of action, efficacy and safety of this novel antidiabetic therapeutic approach.
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