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Child Obes. 2017 Oct 11. doi: 10.1089/chi.2017.0180. [Epub ahead of print]

Prenatal Exposure to Endocrine Disruptors and Reprogramming of Adipogenesis: An Early-Life Risk Factor for Childhood Obesity.

Author information

1
1 Department of Biomedical Research, Armed Forces College of Medicine , Cairo, Egypt .
2
2 Department of Medical Biochemistry, Faculty of Medicine, Ain Shams University , Cairo, Egypt .
3
3 Undergraduate Armed Forces College of Medicine , Cairo, Egypt .

Abstract

Obesity is a global health problem. It is characterized by excess adipose tissue that results from either increase in the number of adipocytes or increase in adipocytes size. Adipocyte differentiation is a highly regulated process that involves the activation of several transcription factors culminating in the removal of adipocytes from the cell cycle and induction of highly specific proteins. Several other factors, including hormones, genes, and epigenetics, are among the most important triggers of the differentiation process. Although the main contributing factors to obesity are high caloric intake, a sedentary lifestyle, and genetic predisposition, strong evidence supports a role for life exposure to environmental pollutants. Endocrine-disrupting chemicals are exogenous, both natural and man-made, chemicals that disrupt the body signaling processes, thus interfering with the endocrine system. Several studies have shown that prenatal exposure to endocrine disruptors modulates the mechanisms, by which multipotent mesenchymal stem cells differentiate into adipocytes. This review discusses adipocytes differentiation and highlights the possible mechanisms of prenatal exposure to endocrine disruptors in reprogramming of adipogenesis and induction of obesity later in life. Therefore, this review provides knowledge that reduction of early life exposure to these chemicals could open the door for new strategies in the prevention of obesity, especially during childhood.

KEYWORDS:

adipogenesis; childhood; endocrine disruptors; obesity; prenatal; reprogramming

PMID:
29019419
DOI:
10.1089/chi.2017.0180
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