ABSTRACT
Noninsulin-dependent diabetes mellitus (NIDDM) is the most common form of diabetes in Western populations. An animal model that has been particularly useful in examining the importance of ß-cell dysfunction in the development of Noninsulin-dependent diabetes mellitus (NIDDM) is the neonatal streptozotocin (STZ) rat. Although all of these models are capable of providing important information on the mechanisms underlying the development of NIDDM, the neonatal STZ model has been the most widely characterized. A key question regarding NIDDM is whether the primary cause is a genetic defect in the insulin-secreting ß-cells of the pancreas (insulin deficiency) or in the insulin-signaling pathway (insulin resistance). Resistance to insulin action is also present in the majority of patients with NIDDM, including patients with borderline glucose intolerance and no evidence of insulin deficiency. Insulin secretion triggered by these metabolic secretagogues is generally defective in the neonatal NIDDM model.
