Obesity and being overweight are linked with a cluster of metabolic and vascular disorders that have been termed the metabolic syndrome. This syndrome promotes the incidence of cardiovascular diseases that are an important public health problem because they represent a major cause of death worldwide. Whereas there is not a universally-accepted set of diagnostic criteria, most expert groups agree that this syndrome is defined by an endothelial dysfunction, an impaired insulin sensitivity and hyperglycemia, dyslipidemia, abdominal obesity and hypertension. Epidemiological studies suggest that the beneficial cardiovascular health effects of diets rich in green tea are, in part, mediated by their flavonoid content, with particular benefits provided by members of this family such as epigallocatechin gallate (EGCG). Although their bioavailability is discussed, various studies suggest that EGCG modulates cellular and molecular mechanisms of various symptoms leading to metabolic syndrome. Therefore, according to in vitro and in vivo model data, this review attempts to increase our understanding about the beneficial properties of EGCG to prevent metabolic syndrome.

Bisphenol A (BPA) is an endocrine disruptor with an oestrogenic activity that is widely produced for the manufacture of polycarbonate plastic, epoxy resin, and thermal paper. Its ubiquitous presence in the environment contributes to broad and continuous human exposure, which has been associated with deleterious health effects. Despite numerous controversial discussions and a lack of consensus about BPA's safety, growing evidence indicates that BPA exposure positively correlates with an increased risk of developing obesity. An updated analysis of the epidemiological, in vivo, and in vitro studies indicates that BPA should be considered an obesogenic environmental compound. Precisely, BPA exposure during all life stages correlates with increased body weight and/or body mass index. Developmental periods that include prenatal, infancy, and childhood appear to be critical windows with increased sensitivity to BPA effects. Finally, blood analysis and in vitro data clearly demonstrate that BPA promotes adipogenesis, lipid and glucose dysregulation, and adipose tissue inflammation, thus contributing to the pathophysiology of obesity. Future prevention efforts should now be employed to avoid BPA exposure, and more research to determine in depth the critical time windows, doses, and impact of long-term exposure of BPA is warranted in order to clarify its risk assessment.