Contribution of Mitochondria to Insulin Secretion by Various Secretagogues
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F22%3A00557977" target="_blank" >RIV/67985823:_____/22:00557977 - isvavai.cz</a>
Result on the web
<a href="https://doi.org/10.1089/ars.2021.0113" target="_blank" >https://doi.org/10.1089/ars.2021.0113</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1089/ars.2021.0113" target="_blank" >10.1089/ars.2021.0113</a>
Alternative languages
Result language
angličtina
Original language name
Contribution of Mitochondria to Insulin Secretion by Various Secretagogues
Original language description
Significance: Mitochondria determine glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells by elevating ATP synthesis. As the metabolic and redox hub, mitochondria provide numerous links to the plasma membrane channels, insulin granule vesicles (IGVs), cell redox, NADH, NADPH, and Ca2+ homeostasis, all affecting insulin secretion.Recent Advances: Mitochondrial redox signaling was implicated in several modes of insulin secretion (branched-chain ketoacid [BCKA]-, fatty acid [FA]-stimulated). Mitochondrial Ca2+ influx was found to enhance GSIS, reflecting cytosolic Ca2+ oscillations induced by action potential spikes (intermittent opening of voltage-dependent Ca2+ and K+ channels) or the superimposed Ca2+ release from the endoplasmic reticulum (ER). The ATPase inhibitory factor 1 (IF1) was reported to tune the glucose sensitivity range for GSIS. Mitochondrial protein kinase A was implicated in preventing the IF1-mediated inhibition of the ATP synthase.Critical Issues: It is unknown how the redox signal spreads up to the plasma membrane and what its targets are, what the differences in metabolic, redox, NADH/NADPH, and Ca2+ signaling, and homeostasis are between the first and second GSIS phase, and whether mitochondria can replace ER in the amplification of IGV exocytosis.Future Directions: Metabolomics studies performed to distinguish between the mitochondrial matrix and cytosolic metabolites will elucidate further details. Identifying the targets of cell signaling into mitochondria and of mitochondrial retrograde metabolic and redox signals to the cell will uncover further molecular mechanisms for insulin secretion stimulated by glucose, BCKAs, and FAs, and the amplification of secretion by glucagon-like peptide (GLP-1) and metabotropic receptors. They will identify the distinction between the hub beta-cells and their followers in intact and diabetic states.
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
2022
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Antioxidants & Redox Signaling
ISSN
1523-0864
e-ISSN
1557-7716
Volume of the periodical
36
Issue of the periodical within the volume
13
Country of publishing house
US - UNITED STATES
Number of pages
33
Pages from-to
920-952
UT code for WoS article
000688204200001
EID of the result in the Scopus database
2-s2.0-85130001667