Hepatic metabolism gene expression and gut microbes in offspring, subjected to in-utero PFOS exposure and postnatal diet challenges

Feng Shi, Delbert Almerick T Boncan, Hin Ting Wan, Ting Fung Chan, Eric Lu Zhang, Keng Po Lai, Chris Kong Chu Wong*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

4 Citations (Scopus)


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.

Original languageEnglish
Article number136196
Number of pages22
Issue numberPart 1
Publication statusPublished - Dec 2022

Scopus Subject Areas

  • Public Health, Environmental and Occupational Health
  • Pollution
  • Chemistry(all)
  • Health, Toxicology and Mutagenesis
  • Environmental Engineering
  • Environmental Chemistry

User-Defined Keywords

  • Body Weight
  • Carbohydrates
  • Diet, High-Fat
  • Fatty Acids, Volatile/metabolism
  • Female
  • Gastrointestinal Microbiome
  • Gene Expression
  • Humans
  • Lipid Metabolism
  • Lipids
  • Liver/metabolism
  • Polysaccharides/metabolism
  • Prenatal Exposure Delayed Effects/metabolism
  • Sucrose/metabolism
  • Vitamins/metabolism


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