The insulin pathway is crucial for the regulation of intracellular and blood glucose levels and the prevention of diabetes. Regulating blood glucose levels demands coordinated interaction between several tissues, which is facilitated by the release of and response to the hormone, insulin. In response to an increase in circulating glucose levels, insulin is secreted by pancreatic beta cells to cause an increase in the uptake of glucose, fatty acids and amino acids into adipose tissue, muscle and the liver to subsequently promote the storage of these nutrients in the form of glycogen, lipids and protein, respectively, as well as suppress hepatic glucose release. Insulin sensitivity is measured by the relative capacity of insulin to promote a decrease in blood glucose. Failure to uptake and store nutrients results in diabetes. Type-1 diabetes is characterized as an autoimmune disease, resulting in destruction of the insulin-producing beta cells and therefore an inability to synthesize insulin. In contrast, in type-2 diabetes, the body develops resistance to the biological actions of insulin, presumably due to defects in the insulin signaling pathway. In this 'Primers on Molecular Pathways', we discuss this important signaling pathway, which is central to pancreas biology.
(c) 2009 S. Karger AG, Basel.