bisphenol A & fetal thyroid-adipokine dysfunction

What is it about?

Because bisphenol A (BPA) has been detected in animals, the aim of this study was to investigate the possible effects of maternal BPA exposure on the fetal endocrine system (thyroid-adipokine axis). BPA (20 or 40 mg/kg body weight) was orally administered to pregnant rats from gestation day (GD) 1e20. In both treated groups, the dams and their fetuses had lower serum thyroxine (T4) and triiodothyronine (T3) levels, and higher thyrotropin (TSH) level than control dams and fetuses at GD 20. Some histopathological changes in fetal thyroid glands were observed in both maternal BPA groups at embryonic day (ED) 20, including fibroblast proliferation, hyperplasia, luminal obliteration, oedema, and degeneration. These disorders resulted in the suppression of fetal serum growth hormone (GH), insulin growth factor-1 (IGF1) and adiponectin (ADP) levels, and the elevation of fetal serum leptin, insulin and tumor necrosis factoralpha (TNFa) levels in both treated groups with respect to control. The depraved effects of both treated groups were associated with reduced maternal and fetal body weight compared to the control group. These alterations were dose dependent. Thus, BPA might penetrate the placental barrier and perturb the fetal thyroid adipokine axis to influence fat metabolism and the endocrine system.

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Why is it important?

this study provides in vivo evidence that both dosage administrations appear to induce maternofetal hypothyroidism via thyroid dysgenesis and dyshormonogenesis. This state seems to alter the fetal adipokine axis, fat metabolism and, in general, prenatal development. Also, the maternal administrations of BPA seem to cause fetal thyroid-adipokine dysfunction. These changes may be either directly or indirectly related to maternofetal TH action.

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