Abstract
Overnutrition and sedentary activity reinforce the growing trend of worldwide obesity, insulin resistance, and type 2 diabetes. However, we have limited insight into how food intake generates sophisticated metabolic perturbations associated with obesity. Accumulation of mitochondrial oxidative stress contributes to the metabolic changes in obesity, but the mechanisms and significance are unclear. In white adipose tissue (WAT), mitochondrial oxidative stress, and the generation of reactive oxygen species (ROS) impact the endocrine and metabolic function of fat cells. The central role of mitochondria in nutrient handling suggests pharmacological targeting of pathological oxidative stress likely improves the metabolic profile of obesity. This review will summarize the critical pathogenic mechanisms of obesity-driven oxidative stress in WAT.
Highlights
Specialty section: This article was submitted to Clinical and Translational Physiology, a section of the journal Frontiers in Physiology
Oxidative stress associates with intra-abdominal obesity and insulin resistance (Furukawa et al, 2004; Frohnert et al, 2011). These results indicate the oxidizing environment in White adipose tissue (WAT) of obese individuals likely impacts fat cell function and energy balance
Systemic oxidative stress and insulin resistance did not coincide with inflammatory cytokines in plasma nor ER stress in WAT. These findings provide a causal link between oxidative stress and insulin resistance in humans
Summary
Overnutrition and sedentary activity reinforce the growing trend of worldwide obesity, insulin resistance, and type 2 diabetes. In white adipose tissue (WAT), mitochondrial oxidative stress, and the generation of reactive oxygen species (ROS) impact the endocrine and metabolic function of fat cells. Obese individuals exhibit higher levels of oxidative stress in WAT, including elevated ROS levels and decreased antioxidant activity coupled with alterations in adipokines required for insulin sensitivity (Furukawa et al, 2004). Oxidative stress associates with intra-abdominal obesity and insulin resistance (Furukawa et al, 2004; Frohnert et al, 2011). These results indicate the oxidizing environment in WAT of obese individuals likely impacts fat cell function and energy balance. Numerous questions remain, including how gradients of ROS inside the cell impact signaling cascades and gene regulation
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