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Review

The Pancreatic β-Cell: The Perfect Redox System

Department of Mitochondrial Physiology, No.75, Institute of Physiology of the Czech Academy of Sciences, 14220 Prague, Czech Republic
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Author to whom correspondence should be addressed.
Academic Editor: Saverio Francesco Retta
Antioxidants 2021, 10(2), 197; https://doi.org/10.3390/antiox10020197
Received: 29 December 2020 / Revised: 20 January 2021 / Accepted: 25 January 2021 / Published: 29 January 2021
(This article belongs to the Special Issue Mitochondrial Redox Regulations)
Pancreatic β-cell insulin secretion, which responds to various secretagogues and hormonal regulations, is reviewed here, emphasizing the fundamental redox signaling by NADPH oxidase 4- (NOX4-) mediated H2O2 production for glucose-stimulated insulin secretion (GSIS). There is a logical summation that integrates both metabolic plus redox homeostasis because the ATP-sensitive K+ channel (KATP) can only be closed when both ATP and H2O2 are elevated. Otherwise ATP would block KATP, while H2O2 would activate any of the redox-sensitive nonspecific calcium channels (NSCCs), such as TRPM2. Notably, a 100%-closed KATP ensemble is insufficient to reach the −50 mV threshold plasma membrane depolarization required for the activation of voltage-dependent Ca2+ channels. Open synergic NSCCs or Cl channels have to act simultaneously to reach this threshold. The resulting intermittent cytosolic Ca2+-increases lead to the pulsatile exocytosis of insulin granule vesicles (IGVs). The incretin (e.g., GLP-1) amplification of GSIS stems from receptor signaling leading to activating the phosphorylation of TRPM channels and effects on other channels to intensify integral Ca2+-influx (fortified by endoplasmic reticulum Ca2+). ATP plus H2O2 are also required for branched-chain ketoacids (BCKAs); and partly for fatty acids (FAs) to secrete insulin, while BCKA or FA β-oxidation provide redox signaling from mitochondria, which proceeds by H2O2 diffusion or hypothetical SH relay via peroxiredoxin “redox kiss” to target proteins. View Full-Text
Keywords: pancreatic β-cells; insulin secretion; redox signaling; NADPH oxidase 4; branched-chain ketoacid oxidation; fatty-acid-stimulated insulin secretion; ATP-sensitive K+ channel; TRPM channels; GLP-1; GPR40 pancreatic β-cells; insulin secretion; redox signaling; NADPH oxidase 4; branched-chain ketoacid oxidation; fatty-acid-stimulated insulin secretion; ATP-sensitive K+ channel; TRPM channels; GLP-1; GPR40
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MDPI and ACS Style

Ježek, P.; Holendová, B.; Jabůrek, M.; Tauber, J.; Dlasková, A.; Plecitá-Hlavatá, L. The Pancreatic β-Cell: The Perfect Redox System. Antioxidants 2021, 10, 197. https://doi.org/10.3390/antiox10020197

AMA Style

Ježek P, Holendová B, Jabůrek M, Tauber J, Dlasková A, Plecitá-Hlavatá L. The Pancreatic β-Cell: The Perfect Redox System. Antioxidants. 2021; 10(2):197. https://doi.org/10.3390/antiox10020197

Chicago/Turabian Style

Ježek, Petr, Blanka Holendová, Martin Jabůrek, Jan Tauber, Andrea Dlasková, and Lydie Plecitá-Hlavatá. 2021. "The Pancreatic β-Cell: The Perfect Redox System" Antioxidants 10, no. 2: 197. https://doi.org/10.3390/antiox10020197

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