Abstract
cute and Chronic Regulation of Mitochondrial Function and Cardiometabolic Disease Risk
Highlights
Obesity and type 2 diabetes (T2D) comprise a growing global burden on healthcare and financial resources, as a function of the Westernization of diets and reduced activity levels across the world
We have recently shown that following a hyperinsulinemiceuglycemic clamp, reactive oxygen species (ROS) production is elevated and mitochondrial coupling is decreased in human skeletal muscle mitochondria measured in permeabilized myofibers from healthy premenopausal women [14]
These data suggest that the increased fatty acid (FA) oxidation observed in obese persons using in vivo methods reflects an adaptation at the mitochondrial level to utilize excess FA substrate, though this phenotype has been shown to become impaired once body mass index (BMI) surpasses 40 kg/m2 [23]
Summary
Obesity and type 2 diabetes (T2D) comprise a growing global burden on healthcare and financial resources, as a function of the Westernization of diets and reduced activity levels across the world. In order to meet the demands of both chronic and acute metabolic challenges and to prevent excessive ROS production, a number of adaptations to mitochondrial physiology and morphology can occur [3].
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