摘要
The Metabolic Syndrome (MetS) is a complex condition which is characterized by increased risk factor for cardiovascular diseases, such as dyslipidemia, hypertension and central obesity, in addition to increased risk for type 2 diabetes mellitus (T2DM). All of these factors alone have a notable relationship with DNA damage. However, when the risks are combined, the extent for major outcomes being related to DNA damage (cancer), the consequence can be accelerated by the metabolic dysfunction. This article will illustrate the scientific evidence of the role of DNA damage in MetS, as well as discuss the interplay of major risks factors (air pollution, physical inactivity and dietary interventions) in genomic stability.
The Metabolic Syndrome (MetS) is a complex condition which is characterized by increased risk factor for cardiovascular diseases, such as dyslipidemia, hypertension and central obesity, in addition to increased risk for type 2 diabetes mellitus (T2DM). All of these factors alone have a notable relationship with DNA damage. However, when the risks are combined, the extent for major outcomes being related to DNA damage (cancer), the consequence can be accelerated by the metabolic dysfunction. This article will illustrate the scientific evidence of the role of DNA damage in MetS, as well as discuss the interplay of major risks factors (air pollution, physical inactivity and dietary interventions) in genomic stability.
