Abstract
Abstract Diabetes is due to the concomitant presence of insulin resistance and impaired insulin secretion. β-Cell dysfunction begins during the prediabetic period, is progressive and not modified by the used therapy. It seems to be determined also by the genetic pattern, and some variants of TCF7L2 gene show in recent reports the strongest association with the alteration of both β-cell function and mass. New therapeutic approaches should therefore improve not only the function but also the β-cell mass. To this aim, strict glycemic control, insulin-sensitizers such as thiazolidinediones and incretin mimetic molecules can be used.
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