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Updated: Aug 2, 2025

Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
Published on: June 28, 2024
Maternal polychlorinated biphenyl 126 (PCB 126) exposure modulates offspring gut microbiota irrespective of diet and
Manisha Agarwal1, Jessie Hoffman2, Sara Y Ngo Tenlep3
1Department of Pharmacology, School of Medicine, Wayne State University, Detroit, MI, 48202, USA.
Insights
Maternal exposure to dioxin-like polychlorinated biphenyls (PCBs) significantly reduced gut microbial diversity in aged offspring. These effects persisted regardless of maternal exercise or offspring diet, impacting key bacteria.
Area of Science:
- Environmental toxicology
- Microbiome research
- Developmental origins of health and disease
Background:
- The gut microbiota is crucial for host health throughout life.
- Maternal exposures before and during pregnancy can influence offspring's microbial communities.
- Polychlorinated biphenyls (PCBs) are environmental contaminants with potential health impacts.
Purpose of the Study:
- To investigate the long-term effects of maternal exposure to dioxin-like PCBs on offspring gut microbiota.
- To determine if maternal exercise or offspring high-fat diet modify these PCB-induced alterations.
- To identify specific microbial taxa affected by maternal PCB exposure.
Main Methods:
- Dams were exposed to PCB 126 or vehicle control during preconception, gestation, and lactation.
- Maternal exercise was implemented using running wheels before and during pregnancy.
- Female offspring were fed either a regular or high-fat diet in adulthood, and their gut microbiota was analyzed using 16S rRNA sequencing.
Main Results:
- Maternal PCB 126 exposure significantly reduced microbial richness and diversity in aged offspring.
- Offspring diet composition influenced overall microbiota structure, but PCB effects were independent of diet or maternal exercise.
- Specific taxa alterations included depletion of Verrucomicrobiaceae and Akkermansia muciniphila, and an increase in Anaeroplasma.
Conclusions:
- Maternal exposure to PCB 126 causes persistent gut dysbiosis in offspring, reducing microbial diversity.
- These PCB-induced microbiota changes may increase susceptibility to chronic diseases later in life.
- Lifestyle factors like diet and exercise did not fully mitigate the negative impacts of maternal PCB exposure on the offspring gut microbiome.
Abstract:
The gut microbiota plays an important role throughout the lifespan in maintaining host health, and several factors can modulate microbiota composition including diet, exercise, and environmental exposures. Maternal microbiota is transferred to offspring during early life; thus, environmental exposures before gestation may also modulate offspring microbiota. Here we aimed to investigate the effects of maternal exposure to dioxin-like polychlorinated biphenyls (PCBs) on the microbiota of aged offspring and to determine if lifestyle factors, including maternal exercise or offspring high-fat feeding alter these associations. To test this, dams were exposed to PCB 126 (0.5 μmole/kg body weight) or vehicle oil by oral gavage during preconception, gestation, and during lactation. Half of each group was allowed access to running wheels for ≥ 7 days before and during pregnancy and up through day 14 of lactation. Female offspring born from the 4 maternal groups (PCB exposure or not, with/without exercise) were subsequently placed either on regular diet or switched to a high-fat diet during adulthood. Microbiota composition was quantified in female offspring at 49 weeks of age by 16 S rRNA sequencing. Maternal exposure to PCB 126 resulted in significantly reduced richness and diversity in offspring microbiota regardless of diet or exercise. Overall compositional differences were largely driven by offspring diet, but alterations in specific taxa due to maternal PCB 126 exposure, included the depletion of Verrucomicrobiaceae and Akkermansia muciniphila, and an increase in Anaeroplasma. Perturbation of microbiota due to PCB 126 may predispose offspring to a variety of chronic diseases later in adulthood.
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