RESEARCH ARTICLE
The Role of Endocrine Disruptors on Metabolic Dysfunction
Diogo Pestana1, 2, Diana Teixeira1, 2, Carla Sá2, Luísa Correia-Sá3, Valentina F. Domingues3, Rosário Monteiro2, 4, Conceição Calhau1, 2, *
Article Information
Identifiers and Pagination:
Year: 2016Volume: 10
Issue: Suppl-1, M9
First Page: 108
Last Page: 121
Publisher ID: TOBIOTJ-10-108
DOI: 10.2174/1874070701610010108
Article History:
Received Date: 20/6/2014Revision Received Date: 22/5/2015
Acceptance Date: 5/6/2015
Electronic publication date: 31/03/2016
Collection year: 2016
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
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.
