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Insulin is produced and secreted by the B cells in the endocrine pancreas. In vivo, insulin secretion is under the control of a number of metabolic, neural and hormonal substances. It is now clear that stimulation of insulin release by fuel secretagogues, such as glucose, involves the closure of K+ channels that are sensitive to the intracellular ATP concentration (KATP channels). This leads to membrane depolarization and the generation of Ca2(+)-dependent action potentials. The mechanisms whereby hormones and neurotransmitters such as adrenaline, galanin and somatostatin, which are released by intraislet nerve endings and the pancreatic D cells, produce inhibition of insulin secretion are not clear. Here we show that adrenaline suppresses B-cell electrical activity (and thus insulin secretion) by a G protein-dependent mechanism, which culminates in the activation of a sulphonylurea-insensitive low-conductance K+ channel distinct from the KATP channel.

Original publication

DOI

10.1038/349077a0

Type

Journal article

Journal

Nature

Publication Date

03/01/1991

Volume

349

Pages

77 - 79

Keywords

Animals, Clonidine, Epinephrine, Glucose, Glyburide, Islets of Langerhans, Membrane Potentials, Mice, Potassium Channels, Tolbutamide, Yohimbine