What question did this study set out to answer?

To evaluate how bisphenol A affects obesity development differently in male and female mice.

May 14, 2026

Sex-Dependent Effects of Bisphenol A Exposure on Obesity Development in Mice

Key Points

To evaluate how bisphenol A affects obesity development differently in male and female mice.
Pregnant CD-1 mice received BPA or control from gestational day 8 to postnatal day 21.
Offspring were assigned to high-fat or low-fat diets based on adiposity index.
Body weight and food intake were measured regularly, with metabolic parameters assessed at ~4 months.
BPA exposure trends toward increased body weight and adiposity index in both sexes, significantly impacting females on low-fat diet (p=0.0181).
Males showed a trend towards increased cumulative food intake after BPA exposure (p=0.0943).
No significant differences in metabolic parameters were observed in indirect calorimetry data.

Abstract

Background: Endocrine-disrupting chemicals are ubiquitous in the environment, and many have been thoroughly established as obesogenic. Limited work has been conducted to examine the role of BPA exposure in utero on the pathogenesis of adulthood metabolic disease. The present study aims to evaluate if in utero exposure predisposes individuals to metabolic disease.Objective: To investigate sex-dependent effects of bisphenol A (BPA), a common endocrine-disrupting chemical, on the development of obesity in mice. We hypothesized that perinatal BPA exposure would cause increased food intake, body weight, and adiposity index in both sexes.Methods: Pregnant CD-1 mice (n = 20) ~10 weeks of age received BPA (~50 µg/kg/day) or control solution via extended-release pellets from gestational day 8 through postnatal day 21. Offspring (two males and two females per litter) were assigned to either a high-fat diet (HFD) or low-fat diet (LFD) on the basis of adiposity index (grams of fat mass / grams of lean mass). Body weight was measured weekly; food intake was measured three times per week; body composition was measured monthly; and metabolic parameters (physical activity and energy expenditure) were assessed using indirect calorimetry at ~4 months of age. Mice were scarified at 6 months of age.Results: Preliminary findings indicate that perinatal BPA exposure is associated with a trend toward increased body weight and adiposity index (adipose mass/lean mass) in both sexes on HFD and females on LFD. Exposure to BPA also caused a trend towards increased cumulative food intake among males (p = 0.0943). In contrast, BPA significantly decreased cumulative food intake in females (p = 0.0181), despite increased trends in adiposity and weight. No significant differences were observed between groups for the indirect calorimetry data.Conclusions: The current results suggest that BPA exposure promotes obesogenic phenotypes in both sexes, but through distinct mechanisms. The anorexigenic response observed in females may reflect BPA’s estrogen-mimicking activity, as estrogen is known to have an anorexic effect. More work will be done to examine the relationship in females, specifically how BPA causes them to eat less but trend towards higher body weight, including different timepoints for indirect calorimetry. Additional cohorts are in progress to increase the power of these analyses, including that for the indirect calorimetry data. Ongoing data collection will further elucidate the mechanistic underpinnings of these findings. Funding: UMN internal grant to CMK. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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