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Trends Endocrinol Metab. 2017 Aug;28(8):612-625. doi: 10.1016/j.tem.2017.05.001. Epub 2017 May 29.

Gut Microbiota, Endocrine-Disrupting Chemicals, and the Diabetes Epidemic.

Author information

1
Department of Molecular Biology, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai 625 021, Tamil Nadu, India. Electronic address: oomvel@gmail.com.
2
Department of Molecular Biology, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai 625 021, Tamil Nadu, India.
3
Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 1213, Lyon, France.
4
KMCH Research Foundation, Kovai Medical Centre and Hospital (KMCH), Coimbatore, Tamil Nadu, India.
5
Department of Molecular Biology, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai 625 021, Tamil Nadu, India. Electronic address: subbiahr@nrcbsmku.org.

Abstract

Diabetes is rapidly emerging as one of the biggest health concerns worldwide, with profound implications for disability, mortality, and costs. This suddenly escalating rate of diabetes correlates with global industrialization and the production of plastics, pesticides, synthetic fertilizers, electronic waste, and food additives that release endocrine-disrupting chemicals (EDCs) into the environment and the food chain. Emerging evidence indicates an association between exposure of EDCs and diabetes. In humans, these chemicals are also metabolized by the gut microbiota and thereby their toxicodynamics are altered. In this review we highlight studies that focus on the role of gut microbiota in EDC-induced hyperglycemia and dysregulated glucose homeostasis. We also discuss the translational implications of understanding EDC-microbiota interactions for the diagnosis and treatment of diabetes.

KEYWORDS:

diabetes epidemic; endocrine-disrupting chemicals; glucose homeostasis; gut microbiota; microbial dysbiosis; microbial metabolism

PMID:
28571659
DOI:
10.1016/j.tem.2017.05.001
[Indexed for MEDLINE]

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