Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat

Abstract

BackgroundThe causes of the current obesity pandemic have not been fully elucidated. Implication of environmental endocrine disruptors such as bisphenol A (BPA) on adipose tissue development has been poorly investigated.ObjectivesThe aim of the present study was to evaluate the effects of perinatal exposure to BPA on early adipose storage at weaning.MethodsPregnant Sprague-Dawley rats had access to drinking water containing 1 mg/L BPA from day 6 of gestation through the end of lactation. Pups were weaned on postnatal day (PND) 21. At that time, we investigated perigonadal adipose tissue of pups (weight, histology, gene expression). For the remaining animals, we recorded body weight and food intake for animals on either standard chow or a high-fat diet.ResultsGestational exposure to BPA did not alter the sex ratio or litter size at birth. On PND1, the weight of male and female BPA-exposed pups was increased. On PND21, body weight was increased only in females, in which parametrial white adipose tissue (pWAT) weight was increased about 3-fold. This excess of pWAT was associated with adipocyte hypertrophy and overexpression of lipogenic genes such as C/EBP-α (CAAT enhancer binding protein alpha), PPAR-γ (peroxisome proliferator-activated receptor gamma), SREBP-1C (sterol regulatory element binding protein-1C), LPL (lipoprotein lipase), FAS (fatty acid synthase), and SCD-1 (stearoyl-CoA desaturase 1). In addition, gene expression of SREBP-1C, FAS, and ACC (acetyl-CoA carboxylase) was also increased in liver from BPA-exposed females at PND21, without a change in circulating lipids and glucose. After weaning, perinatal BPA exposure predisposed to overweight in a sex- and diet-dependent manner. We observed no change in food intake due to perinatal BPA exposure in rats on either standard chow or a high-fat diet.ConclusionsPerinatal exposure to a low dose of BPA increased adipogenesis in females at weaning. Adult body weight may be programmed during early life, leading to changes dependent on the sex and the nutritional status. Although further studies are required to understand the mechanisms of BPA action in early life, these results are particularly important with regard to the increasing prevalence of childhood obesity and the context-dependent action of endocrine disruptors.

Correction and Republication: Effect of Di-(2-ethylhexyl) phthalate on the hypothalamus-pituitary-thyroid axis in adolescent rat

“…The adolescent rats exposed to DEHP resulted higher body weight is identical to others results of study. The available data verified that treated with a low dose of endocrine disruptors during adolescent development can interfere with the normal homeostasis of the endocrine system, and may lead to the occurrence of overweight and obesity [27][28][29]. The function of THs is energy metabolism regulation and the levels of those were decreased with DEHP exposure, this is possible to be a cause for fat accumulation.…”

Alteration Effect of Exendin-4 on Oxidative Stress and Metabolic Disorders Induced by Bisphenol A in Adult Male Mice

“…Body weight increased in all experimental groups, however at the end of the procedure, the treated ones with BPA and exendin-4 had lower weight compared with the control. Some writers revealed a correlation between BPA exposure and body weight elevation (19,20). This result may be explained by the fact that several important mechanisms may affect body weight including, glucose uptakes and homeostasis, adipocyte deposition, dose and duration of treatment, gender and species (21).…”

Bisphenol A: Understanding Its Health Effects from the Studies Performed on Model Organisms

“…In the study by Sakurai et al [71], a high dose of BPA has been revealed to stimulate an increase in the glucose transporter and glucose uptake into adipocytes in cell culture. Study showed that perinatal exposure to a low dose of BPA increased adipogenesis in female rats at weaning [72].…”