Prenatal Bisphenol a Exposure and Postnatal Trans Fat Diet Alter Small Intestinal Morphology and Its Global DNA
Sarah Zulkifli1, Noor Shafina Mohd Nor1,2,3, Siti Hamimah Sheikh Abdul Kadir3,4
1Institute of Medical Molecular Biotechnology, Faculty of Medicine, Universiti Teknologi MARA (UiTM), Cawangan Selangor, Kampus Sungai Buloh, Jalan Hospital, Sungai Buloh 47000, Selangor, Malaysia.
Insights
Prenatal exposure to bisphenol A (BPA) combined with a postnatal trans fat diet (TFD) significantly impacts offspring obesity and small intestine development. BPA exposure alone caused hypermethylation in the small intestine, suggesting complex interactions affecting long-term health.
Area of Science:
- Endocrinology and Metabolism
- Developmental Biology
- Toxicology
Background:
- Prenatal exposure to environmental chemicals like bisphenol A (BPA) is a growing concern.
- The impact of postnatal diets, such as trans fat diets (TFD), on developmental trajectories is not fully understood.
- Interactions between prenatal BPA exposure and postnatal TFD on offspring health require further investigation.
Purpose of the Study:
- To investigate if postnatal trans fat diet (TFD) exacerbates prenatal bisphenol A (BPA) exposure effects on offspring's small intestine and obesity.
- To explore the interaction between BPA and TFD on small intestinal cells and physiological parameters.
- To analyze global DNA methylation and histological changes in the small intestine.
Main Methods:
- Pregnant rats were exposed to BPA or control water.
- Offspring were fed either a normal diet (ND) or TFD from postnatal week 3 to 14.
- Body weight, waist circumference, food/water intake, and small intestine tissues were analyzed.
- Global DNA methylation and histological analyses were performed on small intestinal tissues.
Main Results:
- Offspring exposed to both prenatal BPA and postnatal TFD exhibited significantly higher body weight from postnatal week 9 onwards.
- Ileum crypt length was significantly increased in both BPA-exposed normal diet (BPA-ND) and BPA-TFD groups compared to controls.
- Global small intestinal hypermethylation was observed in the BPA-ND group compared to control groups.
Conclusions:
- Prenatal BPA exposure significantly influences offspring's physiological parameters and intestinal function.
- Postnatal TFD may elicit compensatory responses in offspring with prenatal BPA exposure.
- The combined effects of prenatal BPA and postnatal TFD warrant further research into developmental origins of health and disease.
Abstract:
In this study, we aimed to determine whether a postnatal trans fat diet (TFD) could aggravate prenatal bisphenol A (BPA) exposure effects on offspring’s small intestine and adulthood obesity, due to the relatively sparse findings on how the interaction between these two variables interrupt the small intestinal cells. Twelve pregnant rats were administered with either unspiked drinking water (control; CTL) or BPA-spiked drinking water throughout pregnancy. Twelve weaned pups from each pregnancy group were then given either a normal diet (ND) or TFD from postnatal week (PNW) 3 until PNW14, divided into control offspring on normal diet (CTL-ND), BPA-exposed offspring on normal diet (BPA-ND), control offspring on trans fat diet (CTL-TFD), and BPA offspring on trans fat diet (BPA-TFD) groups. Body weight (BW), waist circumference, and food and water intake were measured weekly in offspring. At PNW14, small intestines were collected for global DNA methylation and histological analyses. Marked differences in BW were observed starting at PNW9 in BPA-TFD (389.5 ± 10.0 g; p < 0.05) relative to CTL-ND (339.0 ± 7.2 g), which persisted until PNW13 (505.0 ± 15.6 g). In contrast, water and food intake between offspring were significantly different (p < 0.01−0.05) at earlier ages only (PNW4−6 and PNW7−9, respectively). Furthermore, substantial differences in the general parameters of the intestinal structures were exclusive to ileum crypt length alone, whereby both BPA-ND (150.5 ± 5.1 μm; p < 0.001), and BPA-TFD (130.3 ± 9.9 μm; p < 0.05) were significantly longer than CTL-ND (96.8 ± 8.9 μm). Moreover, BPA-ND (2.898 ± 0.147%; p < 0.05) demonstrated global small intestinal hypermethylation when compared to CTL-ND and CTL-TFD (1.973 ± 0.232% and 1.913 ± 0.256%, respectively). Prenatal BPA exposure may significantly affect offspring’s physiological parameters and intestinal function. Additionally, our data suggest that there might be compensatory responses to postnatal TFD in the combined BPA prenatal group (BPA-TFD).
