Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitus.
By S. Tangvarasittichai. World Journal of Diabetes, 2015
1,142 citations recorded by the source corpus.
Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus (T2DM) and this appears to underlie the development of cardiovascular disease, T2DM and diabetic complications. Increased oxidative stress appears to be a deleterious factor leading to insulin resistance, dyslipidemia, β-cell dysfunction, impaired glucose tolerance and ultimately leading to T2DM. Chronic oxidative stress, hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant, have high oxidative energy requirements, decrease the gene expression of key β-cell genes and induce cell death. If β-cell functioning is impaired, it results in an under production of insulin, impairs glucose stimulated insulin secretion, fasting hyperglycemia and eventually the development of T2DM.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/2a5d80ebfaf89bbde906bc0031c26d66ef83c280
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In Endocrinology, Diabetes and Metabolism
Citations in the corpus
- Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus (2020, background): “As described before, oxidative stress can impair IST and increase the risk of insulin resistance and DM [26, 34].”
- Mechanisms of Oxidative Stress in Metabolic Syndrome (2023, background): “Adipose tissue is a major source of ROS production as it promotes the generation of superoxide ions in the mitochondrial electron transport chain by inhibiting adenine nucleotide translocation [56], leading to oxidative stress, mitochondrial DNA damage, ATP depletion, and lipotoxicity.”