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Mitochondria to plasma membrane redox signaling is essential for fatty acid β-oxidation-driven insulin secretion

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F24%3A00588550" target="_blank" >RIV/67985823:_____/24:00588550 - isvavai.cz</a>

  • Alternative codes found

    RIV/60461373:22330/24:43929658

  • Result on the web

    <a href="https://doi.org/10.1016/j.redox.2024.103283" target="_blank" >https://doi.org/10.1016/j.redox.2024.103283</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.redox.2024.103283" target="_blank" >10.1016/j.redox.2024.103283</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Mitochondria to plasma membrane redox signaling is essential for fatty acid β-oxidation-driven insulin secretion

  • Original language description

    We asked whether acute redox signaling from mitochondria exists concomitantly to fatty acid- (FA-) stimulated insulin secretion (FASIS) at low glucose by pancreatic β-cells. We show that FA β-oxidation produces superoxide/H2O2, providing: i) mitochondria-to-plasma-membrane redox signaling, closing KATP-channels synergically with elevated ATP (substituting NADPH-oxidase-4-mediated H2O2-signaling upon glucose-stimulated insulin secretion), ii) activation of redox-sensitive phospholipase iPLA2γ/PNPLA8, cleaving mitochondrial FAs, enabling metabotropic GPR40 receptors to amplify insulin secretion (IS). At fasting glucose, palmitic acid stimulated IS in wt mice, palmitic, stearic, lauric, oleic, linoleic, and hexanoic acids also in perifused pancreatic islets (PIs), with suppressed 1st phases in iPLA2γ/PNPLA8-knockout mice/PIs. Extracellular/cytosolic H2O2-monitoring indicated knockout-independent redox signals, blocked by mitochondrial antioxidant SkQ1, etomoxir, CPT1 silencing, and catalase overexpression, all inhibiting FASIS, keeping ATP-sensitive K+-channels open, and diminishing cytosolic [Ca2+]-oscillations. FASIS in mice was a postprandially delayed physiological event. Redox signals of FA β-oxidation are thus documented, reaching the plasma membrane, essentially co-stimulating IS.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30202 - Endocrinology and metabolism (including diabetes, hormones)

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2024

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Redox Biology

  • ISSN

    2213-2317

  • e-ISSN

    2213-2317

  • Volume of the periodical

    75

  • Issue of the periodical within the volume

    September

  • Country of publishing house

    NL - THE KINGDOM OF THE NETHERLANDS

  • Number of pages

    19

  • Pages from-to

    103283

  • UT code for WoS article

    001283528800001

  • EID of the result in the Scopus database

    2-s2.0-85199423143