Whether you eat a whole box of chocolates or fast for the day, your pancreatic beta-cells ensure that your blood glucose level remains relatively constant by regulating the amount of insulin they release. Diabetes results when insulin release is inadequate and consequently blood glucose levels chronically rise. ATP-sensitive potassium (KATP) channels play a vitally important role in regulating insulin secretion by coupling cellular energy metabolism to membrane electrical activity. As a result, mutations in KATP channel genes result in either too much or too little insulin release.

This lecture will describe how the KATP channel regulates insulin secretion. It will show how an understanding of KATP channel function has enabled many patients born with neonatal diabetes to switch from insulin injections to drug therapy, with considerable improvement in both their clinical condition and quality of life. It will also discuss why some KATP channel mutations cause neurological disorders. Finally, it will show how a mouse model of neonatal diabetes has provided fresh insight into the deleterious effects of high blood glucose on pancreatic beta-cells, a finding that has implications for type 2 diabetes and its therapy.