Effects on the liver lipidome of rat offspring prenatally exposed to bisphenol A
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Updated: Nov 28, 2025
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Hoa Thanh Nguyen1, Lingyun Li2, Akifumi Eguchi3
1Center for Marine Environmental Studies, Ehime University, Matsuyama 790-8577, Japan.
Insights
Prenatal exposure to Bisphenol A (BPA) alters lipid profiles in young rats, with effects varying by sex and age. These changes in hepatic lipid homeostasis persist, highlighting BPA
Area of Science:
- Environmental Toxicology
- Metabolomics
- Endocrinology
Background:
- Bisphenol A (BPA) is an endocrine disruptor with known obesogenic effects.
- Previous studies indicated sex- and age-dependent changes in hepatic gene expression after prenatal BPA exposure.
- Understanding BPA's impact on lipid homeostasis is crucial for assessing health risks.
Purpose of the Study:
- To investigate the effects of prenatal Bisphenol A (BPA) exposure on lipidomic profiles in rat offspring.
- To analyze sex- and age-dependent alterations in hepatic lipid metabolism.
- To identify potential lipid biomarkers associated with prenatal BPA exposure.
Main Methods:
- Analysis of lipid profiles in postnatal day (PND) 21 and PND 60 rats using HPLC-QTOF mass spectrometry.
- Quantification of various lipid classes, including fatty acids, acylcarnitines, cholesterol esters, and phospholipids.
- Data Integration Analysis for Biomarker discovery using Latent cOmponents (DIABLO) to correlate lipidome with transcriptome data.
Main Results:
- Prenatal BPA exposure significantly altered lipid content and profiles in a sex- and age-dependent manner.
- Early postnatal changes (PND 21) included increased fatty acids, acylcarnitines, and monoacylglycerols in both sexes, with specific alterations in cholesterol esters, triacylglycerols, and galactolipids in females.
- While some effects on body weight and total lipids diminished by PND 60, lipid profile alterations persisted; DIABLO identified Gpd1 and Gnpat as potential sex-specific biomarkers.
Conclusions:
- Prenatal Bisphenol A (BPA) exposure induces significant, sex- and age-dependent disruptions in hepatic lipid homeostasis.
- Lipidomic alterations persist into later developmental stages, suggesting long-term metabolic consequences.
- The study identified key lipid metabolites and genes (Gpd1, Gnpat) as potential biomarkers for prenatal BPA exposure effects.
Abstract:
Bisphenol A (BPA) is a well-known endocrine disruptor that has obesogenic properties. We have previously reported sex- and age-dependent changes in hepatic transcriptome and proteome of several lipid homeostasis-related genes in rat offspring prenatally exposed to BPA. To further understand the impacts of prenatal BPA exposure, we analyzed lipidomic profiles in the postnatal day (PND) 21 and 60 rats using a high-resolution QTOF mass spectrometer coupled with a HPLC system. We found that the total lipid content was significantly decreased in PND21 females prenatally exposed to 5000 μg/kg bw/day of BPA. Levels of total fatty acids, acylcarnitines, and monoacylglycerols significantly increased in both female and male BPA-exposed rats at PND21. An elevation in total cholesterol esters and reductions in triacylglycerols and monogalactosyl diacylglycerols were found only in PND21 females prenatally exposed to BPA. Interestingly, opposite responses were observed for phospholipids and sphingolipids between PND21 females and males following BPA exposure. The effects on the body weight and total lipid content were mitigated in the latter stage, although the alterations of lipid profiles continued until PND60. A Data Integration Analysis for Biomarker discovery using Latent cOmponents (DIABLO) revealed a high correlation of the lipidome with our previously published transcriptome data. DIABLO also identified potential biomarkers of prenatal exposure to BPA; glycerol-3-phosphate dehydrogenase 1 (Gpd1) and glyceronephosphate O-acyltransferase (Gnpat), which are involved in the glycerophospholipid metabolism, in females and males, respectively. Collectively, we highlighted the sex- and age-dependent effects of prenatal BPA exposure on hepatic lipid homeostasis in rat offspring.
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