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Lipid Dynamics in Pancreatic β-Cells: Linking Physiology to Diabetes Onset

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F24%3A00602189" target="_blank" >RIV/67985823:_____/24:00602189 - isvavai.cz</a>

  • Result on the web

    <a href="https://doi.org/10.1089/ars.2024.0724" target="_blank" >https://doi.org/10.1089/ars.2024.0724</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1089/ars.2024.0724" target="_blank" >10.1089/ars.2024.0724</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Lipid Dynamics in Pancreatic β-Cells: Linking Physiology to Diabetes Onset

  • Original language description

    Significance: Glucose-induced lipid metabolism is essential for preserving functional beta-cells, and its disruption is linked to type 2 diabetes (T2D) development. Lipids are an integral part of the cells playing an indispensable role as structural components, energy storage molecules, and signals.Recent Advances: Glucose presence significantly impacts lipid metabolism in beta-cells, where fatty acids are primarily synthesized de novo and/or are transported from the bloodstream. This process is regulated by the glycerolipid/free fatty acid cycle, which includes lipogenic and lipolytic reactions producing metabolic coupling factors crucial for insulin secretion. Disrupted lipid metabolism involving oxidative stress and inflammation is a hallmark of T2D.Critical Issues: Lipid metabolism in beta-cells is complex involving multiple simultaneous processes. Exact compartmentalization and quantification of lipid metabolism and its intermediates, especially in response to glucose or chronic hyperglycemia, are essential. Current research often uses non-physiological conditions, which may not accurately reflect in vivo situations.Future Directions: Identifying and quantifying individual steps and their signaling, including redox, within the complex fatty acid and lipid metabolic pathways as well as the metabolites formed during acute versus chronic glucose stimulation, will uncover the detailed mechanisms of glucose-stimulated insulin secretion. This knowledge is crucial for understanding T2D pathogenesis and identifying pharmacological targets to prevent this disease.

  • 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

    Antioxidants & Redox Signaling

  • ISSN

    1523-0864

  • e-ISSN

    1557-7716

  • Volume of the periodical

    41

  • Issue of the periodical within the volume

    13-15

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    25

  • Pages from-to

    865-889

  • UT code for WoS article

    001347009200001

  • EID of the result in the Scopus database

    2-s2.0-85209350205