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Insulin Secretion
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The pancreatic cell in a resting state (fasting blood glucose) is hyperpolarized. Glucose, entering via GLUT transporters (primarily GLUT1 in humans, GLUT2 in rodents), is metabolized and elevates cellular ATP, which inhibits. K+ entry through the KATP channel; the decreased K+ conductance results in depolarization, leading to Ca2+- dependent exocytosis of stored insulin. The KATP channel, actually a hetero-octamer composed of SUR1 and Kir 6.2 subunits, is the site of action of several classes of drugs: ATP binds to and inhibits Kir 6.2; sulfonylureas and meglitinides bind to and inhibit SUR1; all 3 agents thereby promote insulin secretion. Diazoxide and ADP-Mg2+ (low ATP) bind to and activate SUR1, thereby inhibiting insulin secretion. Incretins enhance insulin secretion.
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