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Hepatic metabolism gene expression and gut microbes in offspring, subjected to in-utero PFOS exposure and postnatal
Feng Shi1, Delbert Almerick T Boncan2, Hin Ting Wan1
1State Key Laboratory in Environmental and Biological Analysis, Croucher Institute for Environmental Sciences, Department of Biology, Hong Kong Baptist University, Hong Kong SAR, China.
Insights
In-utero exposure to perfluorooctanesulfonic acid (PFOS) disrupts offspring metabolism, leading to altered gut microbiota and increased risk of fatty liver disease. Postnatal diet influences these effects, highlighting the impact of environmental contaminants on metabolic health.
Area of Science:
- Environmental Toxicology
- Developmental Biology
- Metabolomics
Background:
- Perfluorooctanesulfonic acid (PFOS) is a persistent environmental contaminant.
- In-utero exposure to PFOS can impact fetal development and long-term health.
- Understanding PFOS effects on metabolic gene expression and gut microbiota is crucial.
Purpose of the Study:
- To investigate the effects of in-utero PFOS exposure on hepatic metabolic gene expression and gut microbiota in offspring.
- To assess the impact of postnatal diet on PFOS-induced metabolic alterations.
- To determine the association between PFOS exposure, metabolic dysfunction, and hepatic steatosis risk.
Main Methods:
- Animal model exposed to PFOS during gestation.
- Analysis of fetal and postnatal bodyweight, relative liver mass, and lipid accumulation.
- Measurement of hepatic metabolic gene expression.
- 16S rRNA sequencing and metagenomic analysis of cecal microbiota.
- Postnatal diet-challenge (normal diet vs. high-fat diet, with and without sucrose).
Main Results:
- In-utero PFOS exposure decreased fetal bodyweight but increased relative liver mass and lipid accumulation.
- Postnatal catch-up growth observed in high-dose PFOS offspring, with induced hepatic metabolic gene expression and altered gut microbiota (increased carbohydrate catabolism, reduced SCFA metabolism).
- High-fat diet exacerbated metabolic challenges in adult offspring, despite gene upregulation, indicating inefficient fat utilization and reduced microbial biosynthesis of vitamins and SCFAs. Sucrose supplementation mitigated some effects.
Conclusions:
- In-utero PFOS exposure induces lasting metabolic dysregulation in offspring.
- PFOS exposure impairs fat metabolism and increases the risk of hepatic steatosis.
- Gut microbiota alterations play a significant role in mediating PFOS-induced metabolic dysfunction.
Abstract:
We examined the changes in hepatic metabolic gene expression and gut microbiota of offspring exposed to PFOS in-utero. At GD17.5, our data showed that PFOS exposure decreased fetal bodyweights and hepatic metabolic gene expressions but increased relative liver mass and lipid accumulation. At PND21, in-utero high-dose PFOS-exposed offspring exhibited significantly greater bodyweight (catch-up-growth), associated with significant induction of hepatic metabolic gene expression. In addition, 16SrRNA-sequencing of the cecal samples revealed an increase in carbohydrate catabolism but a reduction in microbial polysaccharide synthesis and short-chain fatty acid (SCFA) metabolism. From PND21-80, a postnatal diet-challenge for the offspring was conducted. At PND80 under a normal diet, in-utero high-dose PFOS-exposed offspring maintained the growth "catch-up" effect. In contrast, in a high-fat-diet, the bodyweight of in-utero high-dose PFOS-exposed adult offspring were significantly lesser than the corresponding low-dose and control groups. Even though in the high-fat-diet, the in-utero PFOS-exposed adult offspring showed significant upregulation of hepatic metabolic genes, the lower bodyweight suggests that they had difficulty utilizing high-fat nutrients. Noteworthy, the metagenomic data showed a significant reduction in the biosynthesis of microbial polysaccharides, vitamin B, and SCFAs in the PFOS-exposed adult offspring. Furthermore, the observed effects were significantly reduced in the PFOS-exposed adult offspring with the high-fat diet but supplemented with sucrose. Our study demonstrated that in-utero PFOS exposure caused inefficient fat metabolism and increased the risk of hepatic steatosis in offspring.
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