Summary

The pathological sequence for type 2 diabetes shown in Fig. 1 entails many elements. A genetic predisposition appears to be mandatory, and specific predisposition genes are just beginning to be understood. The diabetes phenotype is then influenced by many environmental factors that share an ability to stress the glucose homeostasis system, either by causing or worsening insulin resistance, or by impairing insulin secretion. Decreased B-cell mass through genetic or cytotoxic factors is a predisposing factor for glucose intolerance, and may be an explanation for "susceptible" B-cells in this disease. Without these predisposing features, the glucose homeostasis system is amazingly adept at maintaining normoglycemia despite poor lifestyle practices. Alternatively, if the blood glucose level rises even a small amount above normal, acquired defects in the glucose homeostasis system occur. Early on, the control of mealtime glycemia is impaired through a reduction in first phase insulin secretion. As the blood glucose rises even more, perhaps in concert with the excess fatty acids that are a typical feature of obesity and insulin resistance, B-cell function deteriorates even further, along with a modest decline in muscle insulin sensitivity and the onset of exaggerated hepatic glucose production. Blood glucose levels then rise to full blown diabetes. This review has presented multiple proposed signaling abnormalities or other pathological processes for the B-cell dysfunction and insulin resistance in type 2 diabetes. None are fully accepted, nor is it likely that a single defect will explain the B-cell dysfunction/death or insulin resistance in this complex disease. Further, it is difficult to understand how cell-based and animal-derived defects relate to humans with type 2 diabetes. Regardless, we can look forward in the next several years to further analysis of the current, as well as new, hypotheses to explain the pathogenesis of type 2 diabetes.

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