Glucose recruits K(ATP) channels via non-insulin-containing dense-core granules

beta cells rely on adenosine triphosphate-sensitive potassium (K(ATP)) channels to initiate and end glucose-stimulated insulin secretion through changes in membrane potential. These channels may also act as a constituent of the exocytotic machinery to mediate insulin release independent of their ele...

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Bibliographic Details
Published in:Cell metabolism 2007-09, Vol.6 (3), p.217-228
Main Authors: Yang, Shao-Nian, Wenna, Nancy Dekki, Yu, Jia, Yang, Guang, Qiu, Hua, Yu, Lina, Juntti-Berggren, Lisa, Köhler, Martin, Berggren, Per-Olof
Format: Article
Language:English
Subjects:
Animals
Calcium - metabolism
Cell Membrane - metabolism
Chromogranins - metabolism
Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors
Cyclic AMP-Dependent Protein Kinases - metabolism
Endocytosis - physiology
Female
Glucose - metabolism
Insulin - metabolism
Insulin-Secreting Cells - cytology
Insulin-Secreting Cells - metabolism
KATP Channels - metabolism
Male
Medicin och hälsovetenskap
Mice
Patch-Clamp Techniques
Potassium Channels, Inwardly Rectifying - metabolism
Protein Subunits - metabolism
Secretory Vesicles - chemistry
Secretory Vesicles - metabolism
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Summary:beta cells rely on adenosine triphosphate-sensitive potassium (K(ATP)) channels to initiate and end glucose-stimulated insulin secretion through changes in membrane potential. These channels may also act as a constituent of the exocytotic machinery to mediate insulin release independent of their electrical function. However, the molecular mechanisms whereby the beta cell plasma membrane maintains an appropriate number of K(ATP) channels are not known. We now show that glucose increases K(ATP) current amplitude by increasing the number of K(ATP) channels in the beta cell plasma membrane. The effect was blocked by inhibition of protein kinase A (PKA) as well as by depletion of extracellular or intracellular Ca(2+). Furthermore, glucose promoted recruitment of the potassium inward rectifier 6.2 to the plasma membrane, and intracellular K(ATP) channels localized in chromogranin-positive/insulin-negative dense-core granules. Our data suggest that glucose can recruit K(ATP) channels to the beta cell plasma membrane via non-insulin-containing dense-core granules in a Ca(2+)- and PKA-dependent manner.
ISSN:1550-4131
DOI:10.1016/j.cmet.2007.08.002