Glucose and GTP-binding protein-coupled receptor cooperatively regulate transient receptor potential-channels to stimulate insulin secretion [Review]

In pancreatic β-cells, glucose-induced closure of the ATP-sensitive K+ (KATP) channel is an initial process triggering glucose-stimulated insulin secretion (GSIS). This KATP-channel dependent pathway has been believed to be a central mechanism for GSIS. However, since the resting membrane potential...

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Bibliographic Details
Published in:ENDOCRINE JOURNAL 2016, Vol.63(10), pp.867-876
Main Authors: Kakei, Masafumi, Yoshida, Masashi, Dezaki, Katsuya, Ito, Kiyonori, Yamada, Hodaka, Funazaki, Shunsuke, Kawakami, Masanobu, Sugawara, Hitoshi, Yada, Toshihiko
Format: Article
Language:English
Subjects:
Animals
Glucose - metabolism
Glucose - physiology
GPCR
GTP-Binding Proteins - metabolism
GTP-Binding Proteins - physiology
Humans
Insulin - metabolism
Insulin Secretion
Insulin-Secreting Cells - metabolism
Pancreatic β-cells
Receptors, G-Protein-Coupled - physiology
Signal Transduction
Transient Receptor Potential Channels - metabolism
Transient Receptor Potential Channels - physiology
TRP channel
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Summary:In pancreatic β-cells, glucose-induced closure of the ATP-sensitive K+ (KATP) channel is an initial process triggering glucose-stimulated insulin secretion (GSIS). This KATP-channel dependent pathway has been believed to be a central mechanism for GSIS. However, since the resting membrane potential of cells is determined by the balance of the net result of current amplitudes in outward and inward directions, it must be taken into consideration that not only KATP channel inhibition but also inward current via the basal opening of non-selective cation channels (NSCCs) plays a crucial role in membrane potential regulation. The basal activity of NSCCs is essential to effectively evoke depolarization in concert with KATP channel closure that is dependent on glucose metabolism. The present study summarizes recent findings regarding the roles of NSCCs in GSIS and GTP-binding protein coupled receptor-(GPCR) operated potentiation of GSIS.
ISSN:0918-8959
1348-4540
DOI:10.1507/endocrj.EJ16-0262