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Review
, 354 (1-2), 74-84

The Estrogenic Endocrine Disrupting Chemical Bisphenol A (BPA) and Obesity

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Review

The Estrogenic Endocrine Disrupting Chemical Bisphenol A (BPA) and Obesity

Frederick S Vom Saal et al. Mol Cell Endocrinol.

Abstract

There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in adult obesity and other components of metabolic syndrome. In particular, there is evidence that epigenetic changes associated with the use of manmade chemicals may interact with other factors that influence fetal and postnatal growth in contributing to the current obesity epidemic. The focus of this review is on the developmental effects of estrogenic endocrine disrupting chemicals (EDCs), and more specifically on effects of exposure to the estrogenic EDC bisphenol A (BPA), on adipocytes and their function, and the ultimate impact on adult obesity; BPA exposure also results in impaired reproductive capacity. We discuss the interaction of EDCs with other factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, and how these influence fetal growth and abnormalities in homeostatic control systems required to maintain normal body weight throughout life.

Figures

Figure 1
Figure 1
Schematic depicting the consequence of intrauterine growth restriction (IUGR) and macrosomia on postnatal growth. There are two trajectories for fetuses that experience IUGR; one sub-group may remain underweight throughout life, while another sub-group may experience overgrowth and obesity in adulthood. The IUGR fetuses differ from normal body weight at birth babies in their response to nutrients, and the postnatal growth trajectory of the different sub-groups of IUGR fetuses depends on factors during postnatal life, as predicted by the “thrifty phenotype” hypothesis. Research indicates that the mechanisms underlying obesity in macrosomic and IUGR individuals are different.
Figure 2
Figure 2
Blood flow (indicated by arrows) into the loop uterine artery is bi-directional from both the ovarian (O) and cervical (C) ends of the uterine horn, which leads to greater placental blood flow at the ends relative to the middle (M) of each uterine horn. The data shown are placental blood flow measurements taken from a hemi-ovariectomized pregnant female CD-1 mouse on gestation day 18; the female was injected with radiolabelled microspheres to measure blood flow [150]. Removing the left ovary prior to pregnancy results in double the number of oocytes being ovulated from the remaining right ovary and crowding in the right uterine horn, which is separate from the left uterine horn in mice and rats.

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