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 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.
Internal Medicine, Saitama Medical Center, Jichi Medical University, Saitama 330-8503, Japan.
Masafumi
M
Kakei
Masashi
M
Yoshida
Katsuya
K
Dezaki
Kiyonori
K
Ito
Hodaka
H
Yamada
Shunsuke
S
Funazaki
Masanobu
M
Kawakami
Hitoshi
H
Sugawara
Toshihiko
T
Yada
D000818:Animals; D019204:GTP-Binding Proteins / Q000378:metabolism / Q000502:physiology*; D005947:Glucose / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000502:physiology*; D015398:Signal Transduction; D050051:Transient Receptor Potential Channels / Q000378:metabolism* / Q000502:physiology
D007328:Insulin; D043562:Receptors, G-Protein-Coupled; D050051:Transient Receptor Potential Channels; D019204:GTP-Binding Proteins; D005947:Glucose