Loss of pulsatile insulin secretion: A factor in the pathogenesis of type 2 diabetes?

摘要

For many years, the prevailing view has been that the initiating event in type 2 diabetes is development of insulin resistance in peripheral tissues that triggers overproduction of insulin by pancreatic beta-cells. Eventually, beta-cells reach a stage at which they are unable to compensate for the insulin resistance, resulting in hyperglycemia and overt diabetes. The underlying cause of tissue insulin resistance is not well understood, but several putative mechanisms including ectopic lipid accumulation and low-grade activation of inflammatory pathways have been proposed (1). Recent evidence suggests that beta-ceIl failure may occur in parallel with the development of insulin resistance (2), and beta-ceIl failure may in itself be a cause of insulin resistance (3).