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Reprod Toxicol. 2017 Mar;68:3-33. doi: 10.1016/j.reprotox.2016.10.001. Epub 2016 Oct 17.

Metabolism disrupting chemicals and metabolic disorders.

Author information

1
National Institute of Environmental Health Sciences, Division of Extramural Research and Training Research Triangle Park, NC, USA. Electronic address: heindelj@niehs.nih.gov.
2
University of California, Department of Developmental and Cell Biology, Irvine CA, USA.
3
University of Louisville, Division of Gastroenterology, Hepatology and Nutrition, Louisville KY, USA.
4
Sheba Medical Center and Tel Aviv University, Tel Aviv, Israel.
5
Instituto Superiore di Sanita, Rome, Italy.
6
University of North Carolina at Chapel Hill, School of Public Health, Chapel Hill NC, USA.
7
Institute of Bioengineering and CIBERDEM, Miguel Hernandez University of Elche, Elche, Alicante, Spain.
8
University of Parma, Department of Neurosciences, Parma, Italy.
9
University of Turin, Department of Neuroscience and Neuroscience Institute Cavalieri Ottolenghi (NICO), Turin, Italy.
10
University of Chicago, Section of Endocrinology, Diabetes and Metabolism, Department of Medicine Chicago, IL, USA.
11
University of Massachusetts, Department of Environmental Health Sciences, School of Public Health & Health Sciences, Amherst, MA, USA.
12
University of Missouri, Department of Biological Sciences, Columbia, MO, USA.

Abstract

The recent epidemics of metabolic diseases, obesity, type 2 diabetes(T2D), liver lipid disorders and metabolic syndrome have largely been attributed to genetic background and changes in diet, exercise and aging. However, there is now considerable evidence that other environmental factors may contribute to the rapid increase in the incidence of these metabolic diseases. This review will examine changes to the incidence of obesity, T2D and non-alcoholic fatty liver disease (NAFLD), the contribution of genetics to these disorders and describe the role of the endocrine system in these metabolic disorders. It will then specifically focus on the role of endocrine disrupting chemicals (EDCs) in the etiology of obesity, T2D and NAFLD while finally integrating the information on EDCs on multiple metabolic disorders that could lead to metabolic syndrome. We will specifically examine evidence linking EDC exposures during critical periods of development with metabolic diseases that manifest later in life and across generations.

KEYWORDS:

Developmental origins of health and disease; Diabetes; Endocrine disruptors; Lipid disorders; Metabolism disruptors; Obesity; Obesogens

PMID:
27760374
PMCID:
PMC5365353
DOI:
10.1016/j.reprotox.2016.10.001
[Indexed for MEDLINE]
Free PMC Article

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