In SDT rats, development of hyperglycemia may be more dependent on decreased insulin secretion than insulin resistance, as shown by the fact that the blood insulin concentration tended to be lower than that in normal SD rats even before the onset of diabetes, and marked hypoinsulinemia developed after the onset of hyperglycemia [8, 9], indicating that this strain of rat is a model of nonobese T2D associated with impaired insulin secretion. This evidence concerns the gene INS and diabetes mellitus.