The Pancreatic beta-Cell: The Perfect Redox System

Kód výsledku v 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>

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

The Pancreatic beta-Cell: The Perfect Redox System

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

The Pancreatic beta-Cell: The Perfect Redox System

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30202 - Endocrinology and metabolism (including diabetes, hormones)

Projekt

<a href="/cs/project/GA20-00408S" target="_blank" >GA20-00408S: Redoxní signalizace beta buněk pankreatu při sekreci inzulinu a v rozvoji diabetu 2. typu</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Antioxidants

ISSN

2076-3921

e-ISSN

2076-3921

Svazek periodika

10

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

CH - Švýcarská konfederace

Počet stran výsledku

59

Strana od-do

197

Kód UT WoS článku

000622064300001

EID výsledku v databázi Scopus

2-s2.0-85099995682