Hormonal
Chronic hyperglycemia and subsequent reactive oxygen species (ROS) production cause pancreatic beta-cell dysfunction and insulin resistance in type 2 diabetes by activating the JNK pathway, which suppresses insulin gene transcription and promotes beta-cell apoptosis.
Focus on managing blood glucose levels to reduce the production of reactive oxygen species, which drives beta-cell damage and insulin resistance. While antioxidants are often marketed for health, current evidence suggests they are not sufficient on their own to treat type 2 diabetes; addressing the root cause (hyperglycemia) is essential.
Under diabetic conditions, chronic hyperglycemia and subsequent augmentation of reactive oxygen species (ROS) deteriorate β-cell function and increase insulin resistance which leads to the aggravation of type 2 diabetes.
Why this rating
The paper is a review article citing numerous animal studies (mice, rats) and cell line experiments, with some human genetic association data, but lacks large-scale randomized controlled trials for the specific mechanistic claims.
Source
Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis
Hideaki Kaneto et al. · Mediators of Inflammation · 2010
DOI 10.1155/2010/453892
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