Table 3.

Oxidative stress and human obesity.

Oxidative stress decreases the release of adiponectin with an increase in TNF-α and PAI-1, thus leading to a prothrombogenic status and insulin resistance (83)

In obese children, the overexpression of NOX-2 and dependent oxidative stress suggests a condition of endothelial dysfunction (82)

Adipocytes produce ROS, thus leading to decreased secretion of insulin by pancreatic β cells which is associated to atherosclerosis and hypertension (83)

Generation of AGEs in response to oxidative stress and hyperglycemia contributes to low-grade inflammation and low levels of adiponectin in the presence of a deficit of soluble RAGEs (87, 88)