Abstract
Abdominal obesity appears to be an important component of the metabolic syndrome (MetS), in which along with insulin resistance, hypertension and dyslipidaemia represents an increased risk for developing cardiovascular diseases and type 2 diabetes (T2D). The aetiology of obesity and its comorbidities is multifactorial, but despite the evidence of traditional contributing factors, the role of environmental toxicants with endocrine disrupting activity has been recently highlighted. Indeed, even small concentrations of these endocrine disrupting chemicals (EDCs) have the ability to cause severe health damages. In this revision, we focused our attention on the mechanisms of action and impact of EDCs exposure as a contributor to the present epidemics of obesity and MetS.The "environmental obesogens" hypothesis associates environmental EDCs to the disruption of energy homeostasis, with recent studies demonstrating the ability of these compounds to modulate the adipocyte biology. On the other hand, the distinct distribution pattern observed between two metabolically distinct AT depots (visceral and subcutaneous) and subsequent repercussion in the aggravation of metabolic dysfunction in a context of obesity, provides accumulating evidence to hypothesise that EDCs might have an important “environmental dysmetabolism” effect.However, in addition to adulthood exposure, the perinatal effects are very important, since it may allow a change in the metabolic programming, promoting the further development of obesity and MetS. Therefore, additional research directed at understanding the nature and action of EDCs will illuminate the connection between health and the environment and the possible effects triggered by these compounds in respect to public health.
Highlights
Worldwide, cardiovascular diseases (CVD) continue to be the major cause of mortality and morbidity, with its incidence increasing alarmingly in the developing world
The term “metabolic syndrome” (MetS) denotes the clustering of risk factors for Type 2 diabetes (T2D) and CVD, and its reduction has become one of the major public health challenges worldwide, as it is mentioned on top of the 21st century civilization diseases list [2 - 5]
The mechanisms by which this perinatal exposure programs the adipose tissue (AT) and endocrine function are under investigation, but it is known that maternal tobacco smoke predisposes human and rat offspring to visceral obesity in early adulthood, possibly by programming AT dysfunction via alterations in the glucocorticoid pathway and development of leptin and insulin resistance [108, 110]
Summary
Cardiovascular diseases (CVD) continue to be the major cause of mortality and morbidity, with its incidence increasing alarmingly in the developing world. In search of relevant effects in humans, several authors found a relationship between exposure of EDCs in the organism and body weight increase through the disruption of normal energy homeostasis control, beginning to designate these compounds as environmental “obesogens” [42].
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