The Pancreatic beta-Cell: The Perfect Redox System
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00541624" target="_blank" >RIV/67985823:_____/21:00541624 - isvavai.cz</a>
Result on the web
<a href="https://www.mdpi.com/2076-3921/10/2/197" target="_blank" >https://www.mdpi.com/2076-3921/10/2/197</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/antiox10020197" target="_blank" >10.3390/antiox10020197</a>
Alternative languages
Result language
angličtina
Original language name
The Pancreatic beta-Cell: The Perfect Redox System
Original language description
Pancreatic beta-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 (K-ATP) can only be closed when both ATP and H2O2 are elevated. Otherwise ATP would block K-ATP, while H2O2 would activate any of the redox-sensitive nonspecific calcium channels (NSCCs), such as TRPM2. Notably, a 100%-closed K-ATP 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 beta-oxidation provide redox signaling from mitochondria, which proceeds by H2O2 diffusion or hypothetical SH relay via peroxiredoxin “redox kiss” to target proteins.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30202 - Endocrinology and metabolism (including diabetes, hormones)
Result continuities
Project
<a href="/en/project/GA20-00408S" target="_blank" >GA20-00408S: Pancreatic beta cell redox signaling in insulin secretion mechanism and type 2 diabetes etiology</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2021
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Antioxidants
ISSN
2076-3921
e-ISSN
2076-3921
Volume of the periodical
10
Issue of the periodical within the volume
2
Country of publishing house
CH - SWITZERLAND
Number of pages
59
Pages from-to
197
UT code for WoS article
000622064300001
EID of the result in the Scopus database
2-s2.0-85099995682