Format

Send to

Choose Destination
Curr Environ Health Rep. 2017 Jun;4(2):208-222. doi: 10.1007/s40572-017-0137-0.

Polluted Pathways: Mechanisms of Metabolic Disruption by Endocrine Disrupting Chemicals.

Author information

1
Section of Endocrinology, Diabetes, and Metabolism; Department of Medicine, University of Chicago, Chicago, IL, USA.
2
Institute of Bioengineering and Centro de Investigacion Biomedica en Red de Diabetes y Enfermedades Metabolicas Asociadas, CIBERDEM, Universidad Miguel Hernández de Elche, Alicante, Spain.
3
Division of Endocrinology, Diabetes, and Metabolism; Department of Medicine, University of Illinois at Chicago, 835 S. Wolcott, Suite 625E M/C 640, Chicago, IL, USA. rsargis@uic.edu.

Abstract

PURPOSE OF REVIEW:

Environmental toxicants are increasingly implicated in the global decline in metabolic health. Focusing on diabetes, herein, the molecular and cellular mechanisms by which metabolism disrupting chemicals (MDCs) impair energy homeostasis are discussed.

RECENT FINDINGS:

Emerging data implicate MDC perturbations in a variety of pathways as contributors to metabolic disease pathogenesis, with effects in diverse tissues regulating fuel utilization. Potentiation of traditional metabolic risk factors, such as caloric excess, and emerging threats to metabolism, such as disruptions in circadian rhythms, are important areas of current and future MDC research. Increasing evidence also implicates deleterious effects of MDCs on metabolic programming that occur during vulnerable developmental windows, such as in utero and early post-natal life as well as pregnancy. Recent insights into the mechanisms by which MDCs alter energy homeostasis will advance the field's ability to predict interactions with classical metabolic disease risk factors and empower studies utilizing targeted therapeutics to treat MDC-mediated diabetes.

KEYWORDS:

Diabetes; EDCs; Endocrine disruptor; Glucose intolerance; Insulin resistance; MDCs; Metabolic syndrome; Metabolism; Obesity

PMID:
28432637
PMCID:
PMC5921937
DOI:
10.1007/s40572-017-0137-0
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Springer Icon for PubMed Central
Loading ...
Support Center