Endothelial Dysfunction in Obese Children

Abstract

The magnitude of lifetime risk of cardiovascular disease (CVD) has radically increased along with the high prevalence of obesity in children. The risk factors emerge quite early in the clinical course of obesity, which might have important consequences for the development of atherosclerosis later in life. Endothelial dysfunction represents a key early step in the development of atherosclerosis and is also involved in plaque progression and the occurrence of atherosclerotic complications. Endothelial changes are known to commence in childhood and are present in severely obese children. In endothelial dysfunction, there is a reduction in the bioavailability of vasodilators whereas endothelial derived contracting factors are increased; aside from that there is a state of ‘Endothelial activation’ that favors all stages of atherogenesis. Insulin resistance and the presence of a proinflammatory state are two likely mechanisms that link obesity to endothelial dysfunction. Endothelial dysfunction is a reversible disorder, pharmacological and non pharmacological interventions can reverse the changes. Weight loss leads to an attenuation of the proinflammatory state and the physical exercise increases the synthesis and release of nitric oxide, which leads to augmented flow-mediated dilation and improvement in endothelial function. These changes are consistent with a decreased risk of atherosclerotic progression and reduced risk of cardiovascular disease in obese children. Obesity is associated with both endothelial dysfunction and increased risk of CVD. Measurement of endothelial dysfunction in children can predict the onset of atherosclerosis. Non pharmacological and pharmacological interventions targeting obesity can improve clinical cardiovascular outcomes in obese children.

Keywords

• atherosclerosis
• cardiovascular disease (cvd)
• endothelial dysfunction
• endothelial activation
• insulin resistance
• nitric oxide
• obesity