Abstract
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)1. This leads to membrane depolarization and the generation of Ca2+-dependent action potentials2. 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 clear3. 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.
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Rorsman, P., Bokvist, K., Ämmälä, C. et al. Activation by adrenaline of a low-conductance G protein-dependent K+ channel in mouse pancreatic B cells. Nature 349, 77–79 (1991). https://doi.org/10.1038/349077a0
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DOI: https://doi.org/10.1038/349077a0
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