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. 2025 Feb:495:117188.
doi: 10.1016/j.taap.2024.117188. Epub 2024 Dec 6.

An oat fiber intervention for reducing PFAS body burden: A pilot study in male C57Bl/6 J mice

Jennifer J Schlezinger  1 , Kushal Biswas  2 , Audrey Garcia  3 , Wendy J Heiger-Bernays  4 , Dhimiter Bello  2
Affiliations

An oat fiber intervention for reducing PFAS body burden: A pilot study in male C57Bl/6 J mice

Jennifer J Schlezinger et al. Toxicol Appl Pharmacol. 2025 Feb.

Abstract

Perfluoroalkyl substances (PFAS) are a major public health concern, in part because several PFAS have elimination half-lives on the order of years and are associated with adverse health outcomes. While PFAS can be transported into bile, their efficient reuptake by intestinal transporter proteins results in minimal fecal elimination. Here, we tested the hypothesis that consumption of oat β-glucan, a dietary supplement known to disrupt the enterohepatic recirculation of bile acids, will reduce PFAS body burdens. Male C57Bl/6 J mice were fed diets based on the "What we eat in America" analysis that were supplemented with inulin or oat β-glucan and exposed via drinking water to a seven PFAS mixture (PFHpA, PFOA, PFNA, Nafion Byproduct-2, PFHxS and PFOS) for 6 weeks. One cohort of mice was euthanized at the end of the exposure, and one cohort continued on the experimental diets for 4 more weeks without additional PFAS exposure. The β-glucan fed mice drank significantly more water than the inulin fed mice, resulting in a significantly higher dose of PFAS. Relative to overall exposure, we observed lower serum concentration trends (p < 0.1) in β-glucan fed mice for PFHpA, PFOA and PFOS. Additionally, β-glucan fed mice had lower adipose:body weight ratios and liver and jejunum triglyceride concentrations. Hepatic mRNA expression of Cyp4a10, Cyp2b10 and Cyp3a11 were elevated in PFAS exposed mice, with only the expression of Cyp3a11 decreasing following depuration. This pilot study generates support for the hypothesis that oat β-glucan supplementation can reduce PFAS body burdens and stimulate healthful effects on lipid homeostasis.

Keywords: Dietary fiber; Excretion; Oat beta-glucan; PFAS.

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Conflict of interest statement

Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:

Figures

Figure 1.
Figure 1.. Effect of diet on food and water consumption.
Three-week-old male C57BL6/J mice were treated with either vehicle (Vh, NERL water with 5% sucrose) or PFAS drinking water for 6 weeks. After 6 weeks, one cohort of mice was euthanized and one cohort of mice continued in the experiment for 4 additional weeks with all mice receiving Vehicle water and continuing on their assigned diet. During treatment and depuration, the mice were fed an American Diet supplemented with either inulin or β-glucan (see Table 1). Food and water consumption were determined on a per cage basis weekly and then divided by the total weight of the mice in the cage and by 7 days to determine the consumption rate per gram of mouse. One mouse in the β-glucan-PFAS group drank significantly more water than all other β-glucan mice (24.5 mg/g mouse vs. 5.5 ml/g mouse, respectively), was moved to single housing and was not included in the calculation for this analysis. The vertical dashed line indicates when exposure ended. Data are presented as mean ± SD. N = 3–4 cages. Diet significantly increased water consumption (p = 0.0185, Two-Factor Repeated Measures ANOVA).
Figure 2.
Figure 2.. Estimate of total PFAS dose in mice consuming inulin and β-glucan diets.
Mice were exposed to Vh and PFAS drinking water and fed diets as described in Figure 1. Total PFAS exposure was estimated by calculating the total water consumed per g of mouse over the six-week exposure period (specific to the cage each mouse was in). Water consumption was then multiplied by the concentration of each PFAS in drinking water and exposure summed across PFAS (PFHpA, PFOA, PFNA, PFHxS, PFOS, NBP-2, PFOSA, PFHpA). Data are presented as mean ± SD. Data are based on 4 mice in the inulin group and 3 mice in the β-glucan group. One mouse in the β-glucan group drank significantly more water than all other mice, was moved to single housing and was not included in the calculation. The total exposure in that mouse was estimated to be 45,594 μg/kg. *** - Significantly different from inulin (p < 0.0002, two-tailed, unpaired, Student’s t test).
Figure 3.
Figure 3.. Effect of diet on serum concentrations of PFAS.
Mice were exposed to Vh and PFAS drinking water and fed diets as described in Figure 1. A. Total exposure to each PFAS was calculated as described in Figure 2. The serum PFAS concentration, determined in each mouse, was then divided by the total exposure estimate for that mouse. B. Effects of die and time (exposure vs depuration) on PFAS serum concentrations were tested using a Two-Factor ANOVA. * p<0.05 (Šídák’s test). Data are from individual mice, with the mean indicated by a line. N = 3–4. Abbreviations: Exposure cohort (Expo), depuration cohort (Dep).
Figure 4.
Figure 4.. Effect of diet and PFAS exposure on body weight gain (A) and adiposity (B).
Mice were exposed to Vh and PFAS drinking water and fed diets as described in Figure 1. At euthanasia, (total body weight (6-week exposure and 4-week depuration groups) and perigonadal adipose tissue weight (4-week depuration group) were determined. Data are from individual mice. N = 3–4. Effects of treatment and time (exposure vs depuration) on weight gain for each diet were tested using a Two-Factor ANOVA (time contributed 33–41% of the variation, p<0.05). Effects of diet and treatment on adiposity were tested using a Two-Factor ANOVA (treatment contributed 70% of the variation, p<0.0001). * p<0.05, *** p<0.001 (Šídák’s test). Abbreviations: Exposure cohort (Expo), depuration cohort (Dep)
Figure 5.
Figure 5.. Effect of diet and PFAS exposure on liver weights (A) and triglyceride content (B).
Mice were exposed to Vh and PFAS drinking water and fed diets as described in Figure 1. A. At euthanasia, total body weight and liver weights were determined. B. Total triglyceride concentrations were determined from measuring triolein content in saponified liver extracts. C. Effects of diet, treatment and time (exposure vs depuration) on liver:body weights and liver triglycerides were tested using a Three-Factor ANOVA. ** p<0.01, **** p<0.0001 (Šídák’s test). Data are from individual mice. N = 3–4. Abbreviations: Exposure cohort (Expo), depuration cohort (Dep) and treatment (Tx)
Figure 6.
Figure 6.. Effect of diet and PFAS exposure on triglyceride accumulation in intestine.
Mice were exposed to Vh and PFAS drinking water and fed diets as described in Figure 1. A. Total triglyceride concentrations were determined from measuring triolein content in saponified neutralized jejunum extracts. B. Effects of diet, treatment and time (exposure vs depuration) on organ weights were tested using a Three-Factor ANOVA. Data are from individual mice. N = 3–4. Abbreviations: Exposure cohort (Expo), depuration cohort (Dep) and treatment (Tx).
Figure 7.
Figure 7.. Effect of diet and PFAS exposure on liver nuclear receptor-related gene expression.
Mice were exposed to Vh and PFAS drinking water and fed diets as described in Figure 1. Following isolation of RNA from liver, gene expression was determined by RT-qPCR. A. Ppara and its target gene. B. Nr1i3 and its target gene. C. Nr1i2 and its target gene. D. Effects of diet, treatment and time (exposure vs depuration) on organ weights were tested using a Three-Factor ANOVA. * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001 (Šídák’s test). Data are from individual mice. N = 3–4. Abbreviations: Exposure cohort (Expo), depuration cohort (Dep) and treatment (Tx)
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