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Updated: Jun 17, 2026
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Perinatal exposure to bisphenol a alters early adipogenesis in the rat
Emmanuel Somm1, Valérie M Schwitzgebel, Audrey Toulotte
1Faculty of Medicine, University of Geneva, Geneva, Switzerland. emmanuel.somm@medecine.unige.ch
Insights
Perinatal exposure to bisphenol A (BPA) significantly increased fat storage in female rat pups by weaning. This early exposure may program later overweight risk, highlighting BPA
Area of Science:
- Endocrinology
- Developmental Biology
- Toxicology
Background:
- The obesity pandemic's causes remain unclear, with limited research on endocrine disruptors like bisphenol A (BPA) impacting adipose tissue development.
- Environmental endocrine disruptors are implicated in metabolic disorders, necessitating investigation into their effects on early life adipogenesis.
Purpose of the Study:
- To investigate the effects of perinatal exposure to a low dose of bisphenol A (BPA) on adipose tissue development in rat pups at weaning.
- To evaluate the potential for early-life exposure to endocrine disruptors to influence long-term metabolic programming.
Main Methods:
- Pregnant rats received BPA (1 mg/L) from gestation day 6 through lactation.
- Pups were assessed at postnatal day 21 (weaning) for perigonadal adipose tissue weight, histology, and gene expression.
- Post-weaning body weight and food intake were monitored under standard or high-fat diet conditions.
Main Results:
- Perinatal BPA exposure increased pup weight on postnatal day 1 and female body weight on postnatal day 21.
- Female pups exhibited a 3-fold increase in parametrial white adipose tissue (pWAT) weight, with adipocyte hypertrophy and increased lipogenic gene expression.
- Liver gene expression of key lipogenic enzymes was elevated in BPA-exposed females; post-weaning overweight risk was sex- and diet-dependent.
Conclusions:
- Perinatal exposure to low-dose BPA promotes adipogenesis in female offspring at weaning, suggesting early-life programming of metabolic outcomes.
- These findings underscore the potential role of endocrine disruptors in the rising prevalence of childhood obesity and highlight context-dependent effects.
Background:
The 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.
Objectives:
The aim of the present study was to evaluate the effects of perinatal exposure to BPA on early adipose storage at weaning.
Methods:
Pregnant 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.
Results:
Gestational 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-alpha (CAAT enhancer binding protein alpha), PPAR-gamma (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.
Conclusions:
Perinatal 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.
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