Chapter 2 - Genetics of Oxidative Stress and Obesity-Related Diseases

Abstract

The link between obesity and oxidative stress relies not only on oxidative damage of cellular structures and machinery. Additionally, genetic variants have shown to contribute to this relationship through the alteration of function and levels of enzymes involved in different cellular processes related to oxidative stress. Moreover, the consequences of obesity-associated oxidative stress are also mediated through transcription factor regulatory mechanisms. Reactive oxygen species are able to trigger key cellular signaling pathways, which partly explains the onset of obesity-associated metabolic disturbances such as insulin resistance and metabolic syndrome. In addition, the cell's antioxidant defense system is also affected as seen through disturbed expression of enzymes involved in the protection against oxidative stress. Moreover, epigenetic modifications such as microRNA dysregulation, DNA methylation, and histone acetylation are also shown to be present as inducers and mediators of obesity-associated systemic oxidative stress, atherosclerosis, nonalcoholic fatty liver disease, and even cancer.