Document Type : Narrative Review
Authors
1
Department of Veterinary Sciences, Shabestar Branch, Islamic Azad University, Shabestar, Iran.
2
School of Medicine, Imperial College, London, United Kingdom
3
Department of Physiology, Tabriz Branch, Islamic Azad University, Tabriz, Iran.
4
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
10.30491/ijmr.2024.433426.1272
Abstract
Oxidative stress is one of the most important causes of type 2 diabetes; it impairs the functioning of lipids, proteins, and DNA and can disrupt insulin secretion. Endoplasmic reticulum stress is involved in β-cell dysfunction, and a number of pathways, known as the unfolded protein response, are activated to reduce this stress and protect β-cells from death. Increased autophagy provides a preventative mechanism, protecting against oxidative stress in pancreatic β-cells. Mitochondrial adenosine triphosphate regulates insulin levels, and mitochondrial reactive oxygen species can disrupt insulin secretion. Inflammation is caused by cell damage and is specified by the invasion of immune cells and the local release of cytokines and chemokines. Tumor necrosis factor-α is a proinflammatory cytokine that is produced by adipose tissue during islet inflammation in patients with obesity and insulin resistance, which is associated with lipid peroxidation and oxidative damage to DNA. Inflammation plays a role in the development of insulin resistance, leading to type 2 diabetes. There is a connection between vitamin D deficiency, and decreased insulin secretion, and the pathogenesis of type 2 diabetes. The oxidative damage is also associated with low-grade chronic inflammation and is a risk factor in the pathogenesis of diabetes, which is reviewed in this article.
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