Abstract
The Spontaneously Diabetic Torii (SDT) rat is a useful animal model of type 2 diabetes mellitus without obesity. The diabetes in this model manifests as severe hyperglycemia and hypoinsulinemia. However, insulin treatment is not required for survival despite marked hyperglycemia. Pancreatic islets display unique pathologic changes such as hemorrhage and fibrosis before the onset of hyperglycemia as well as marked atrophy. Islet injury is associated with macrophage infiltration of the islets and excess production of nitric oxide. Impaired glucose tolerance results from impaired insulin secretion following by decrease in beta cell mass and glucose-stimulated insulin release from beta cells. Beta cells in these animals have low insulin-secreting capacity in response to glucose stimulation, but retain normal responses to sulfonylurea and incretin. Although insulin resistance is less presented by body composition without obesity, the SDT rat has the potential contributions of hepatic insulin resistance and low energy expenditure to the development of diabetes. This article provides an overview of the pathologic features of pancreatic islets such as beta cell function and possible insulin resistance in SDT rats.
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