AI Article Synopsis

  • * Increased calorie consumption raises levels of fatty acids in the blood, causing lipotoxicity that damages pancreatic β-cells and impairs their function.
  • * The review highlights the role of oxidative stress from the NADPH oxidase enzyme and its connection to endoplasmic reticulum stress in contributing to β-cell dysfunction and failure in T2D.

Article Abstract

A high caloric intake, rich in saturated fats, greatly contributes to the development of obesity, which is the leading risk factor for type 2 diabetes (T2D). A persistent caloric surplus increases plasma levels of fatty acids (FAs), especially saturated ones, which were shown to negatively impact pancreatic β-cell function and survival in a process called lipotoxicity. Lipotoxicity in β-cells activates different stress pathways, culminating in β-cells dysfunction and death. Among all stresses, endoplasmic reticulum (ER) stress and oxidative stress have been shown to be strongly correlated. One main source of oxidative stress in pancreatic β-cells appears to be the reactive oxygen species producer NADPH oxidase (NOX) enzyme, which has a role in the glucose-stimulated insulin secretion and in the β-cell demise during both T1 and T2D. In this review, we focus on the acute and chronic effects of FAs and the lipotoxicity-induced β-cell failure during T2D development, with special emphasis on the oxidative stress induced by NOX, the ER stress, and the crosstalk between NOX and ER stress.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8699655PMC
http://dx.doi.org/10.3390/cells10123328DOI Listing

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