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

Kód výsledku v 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>

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30202 - Endocrinology and metabolism (including diabetes, hormones)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2024

Kód důvěrnosti údajů

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

Název periodika

Antioxidants & Redox Signaling

ISSN

1523-0864

e-ISSN

1557-7716

Svazek periodika

41

Číslo periodika v rámci svazku

13-15

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

25

Strana od-do

865-889

Kód UT WoS článku

001347009200001

EID výsledku v databázi Scopus

2-s2.0-85209350205