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
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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
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