The genetic basis of the common late-onset diabetes mellitus type 2 is rather polygenic than monogenic. Clinically overt diabetes is characterized by two pathophysiological phenomenon, i.e., reduced insulin sensitivity or insulin resistance and a P-cell dysfunction with diminished insulin secretion. Even if impaired insulin sensitivity is the earliest detectable parameter, diabetes generally manifests when insulin secretion is decreased (2-4). On the survey for genetic factors responsible for an impaired insulin secretion no specific gene or mutation has been identified for late-onset diabetes mellitus type 2 up to now. Nevertheless, during the past decades a great effort has been made to identify monogenic sub-classifications of diabetes as the cause for P-cell dysfunction. The identification of these monogenetic forms of diabetes lead to a paradigm change influencing especially the pediatric physicians to determine the genetic cause of early-onset diabetes and distinguish between type I diabetes and the early-onset monogenetic diabetes forms.
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