Abstract
Metabolic syndrome (MetS) is a worldwide public health issue characterized by a set of risk factors for cardiovascular disease. MetS can originate in early life by developmental programming. Increasing evidence suggests that oxidative stress, which is characterized as an imbalance between reactive oxygen species (ROS), nitric oxide (NO), and antioxidant systems, plays a decisive role in MetS programming. Results from human and animal studies indicate that maternal-derived insults induce MetS later in life, accompanied by oxidative stress programming of various organ systems. On the contrary, perinatal use of antioxidants can offset oxidative stress and thereby prevent MetS traits in adult offspring. This review provides an overview of current knowledge about the core mechanisms behind MetS programming, with particular focus on the occurrence of oxidative-stress-related pathogenesis as well as the use of potential oxidative-stress-targeted interventions as a reprogramming strategy to avert MetS of developmental origins. Future clinical studies should provide important proof of concept for the effectiveness of these reprogramming interventions to prevent a MetS epidemic.