Hormonal
Oxidative stress, generated by mitochondrial overproduction of superoxide due to glucose and free fatty acid overload, is the common pathogenic mechanism linking insulin resistance, beta-cell dysfunction, and endothelial dysfunction, thereby driving the progression from insulin resistance to type 2 diabetes and cardiovascular disease.
Focus on reducing cellular stress, not just blood sugar. This involves managing caloric intake and increasing physical activity to prevent the overload of glucose and fatty acids in cells, which generates damaging oxidative stress. This approach may help prevent both diabetes and cardiovascular disease by addressing the root cause of cellular dysfunction.
Because evidence suggests that overnutrition, insulin resistance, IGT, diabetes, and CVD share in common the presence of an oxidative stress, in this article oxidative stress generation is proposed as the common persistent pathogenic factor mediating the appearance of insulin resistance as well as the passage from insulin resistance to overt diabetes, via IGT, while producing the increased cardiovascular risk condition typical of prediabetic and diabetic subjects by favoring atherosclerotic complications.
Why this rating
The paper is a review/hypothesis paper citing various in vitro, animal, and clinical studies, but does not present new primary clinical trial data itself.
Source
Is Oxidative Stress the Pathogenic Mechanism Underlying Insulin Resistance, Diabetes, and Cardiovascular Disease? The Common Soil Hypothesis Revisited
Antonio Ceriello et al. · Arteriosclerosis Thrombosis and Vascular Biology · 2004
DOI 10.1161/01.atv.0000122852.22604.78
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