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The role and mechanism of VDAC1 in type 2 diabetes: An underestimated target of environmental pollutants.

Authors :
Ma, Yu
Sun, Xiance
Yao, Xiaofeng
Source :
Mitochondrion. Sep2024, Vol. 78, pN.PAG-N.PAG. 1p.
Publication Year :
2024

Abstract

• VDAC1 is deeply involved in the toxic effect of environmental pollutants. • Association of VDAC1 monomers and oligomers with T2D. • VDAC1 affects insulin secretion and insulin resistance. • VDAC1 plays a bridging role in organelle crosstalk. • VDAC1 is a potential target for the prevention of pollutants-related T2D. Type 2 diabetes (T2D) is a chronic metabolic disease that accounts for more than 90% of diabetic patients. Its main feature is hyperglycemia due to insulin resistance or insulin deficiency. With changes in diet and lifestyle habits, the incidence of T2D in adolescents has burst in recent decades. The deterioration in the exposure to the environmental pollutants further aggravates the prevalence of T2D, and consequently, it imposes a significant economic burden. Therefore, early prevention and symptomatic treatment are essential to prevent diabetic complications. Mitochondrial number and electron transport chain activity are decreased in the patients with T2D. Voltage-Dependent Anion Channel 1 (VDAC1), as a crucial channel protein on the outer membrane of mitochondria, regulates signal transduction between mitochondria and other cellular components, participating in various biological processes. When VDAC1 exists in oligomeric form, it additionally facilitates the entry and exit of macromolecules into and from mitochondria, modulating insulin secretion. We summarize and highlight the interplay between VDAC1 and T2D, especially in the environmental pollutants-related T2D, shed light on the potential therapeutic implications of targeting VDAC1 monomers and oligomers, providing a new possible target for the treatment of T2D. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15677249
Volume :
78
Database :
Academic Search Index
Journal :
Mitochondrion
Publication Type :
Academic Journal
Accession number :
179529449
Full Text :
https://doi.org/10.1016/j.mito.2024.101929