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Dietary Components in the Brain–Gut Axis: Exploring Nutrigenetic and Microbiome Interactions

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (30 January 2026) | Viewed by 3954

Special Issue Editor


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Guest Editor
Department Functional Anatomy and Cytobiology, Maria Curie-Sklodowska University, Akademicka 19, 20-033 Lublin, Poland
Interests: bone and cartilage histology; bone implants; cartilage regeneration; glutamine; alpha ketoglutaric acid; nutrients; supplementation; probiotics; microbiome; brain-gut axis; digestive system; high-fat diets; histomorphometry
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Special Issue Information

Dear Colleagues,

This Special Issue aims to explore the complex interplay between dietary components, the brain–gut axis, and the microbiome with a focus on nutrigenetics. It seeks to unravel how dietary components, including carbohydrates, proteins, fats, vitamins, and minerals, influence not only the digestive system but also neurological health, with an expanded view of developmental disorders and obesity. This issue will delve into the metabolic pathways through which dietary components affect both the nervous and digestive systems and their pivotal role in the microbiota–gut–brain axis. This is especially pertinent for understanding the ethology and progression of neurodegenerative diseases, gastrointestinal disorders, developmental disorders, and obesity-related complications. The objective of this Special Issue is to bridge significant gaps in the literature, particularly in the areas of molecular mechanisms, genetic modifiers, and the interplay between diet, microbiome, and disease states. The goal is to present a comprehensive overview of the current research and identify new avenues for exploring the impact of nutrients on a wide range of health conditions and diseases.

Dr. Piotr Dobrowolski
Guest Editor

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Keywords

  • dietary components
  • carbohydrates
  • proteins
  • fats
  • fatty acids
  • vitamins
  • minerals
  • brain–gut axis
  • nutrigenetics
  • microbiome interactions
  • neurodegenerative disorders
  • metabolic pathways

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Published Papers (2 papers)

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Research

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17 pages, 6407 KB  
Article
An In Vivo Model of Propionic Acid-Rich Diet-Induced Gliosis and Neuro-Inflammation in Mice (FVB/N-Tg(GFAPGFP)14Mes/J): A Potential Link to Autism Spectrum Disorder
by Piotr P. Lagod, Latifa S. Abdelli and Saleh A. Naser
Int. J. Mol. Sci. 2024, 25(15), 8093; https://doi.org/10.3390/ijms25158093 - 25 Jul 2024
Cited by 13 | Viewed by 2447
Abstract
Evidence shows that Autism Spectrum Disorder (ASD) stems from an interplay of genetic and environmental factors, which may include propionic acid (PPA), a microbial byproduct and food preservative. We previously reported that in vitro treatment of neural stem cells with PPA leads to [...] Read more.
Evidence shows that Autism Spectrum Disorder (ASD) stems from an interplay of genetic and environmental factors, which may include propionic acid (PPA), a microbial byproduct and food preservative. We previously reported that in vitro treatment of neural stem cells with PPA leads to gliosis and neuroinflammation. In this study, mice were exposed ad libitum to a PPA-rich diet for four weeks before mating. The same diet was maintained through pregnancy and administered to the offspring after weaning. The brains of the offspring were studied at 1 and 5 months postpartum. Glial fibrillary acidic protein (astrocytic marker) was significantly increased (1.53 ± 0.56-fold at 1 M and 1.63 ± 0.49-fold at 5 M) in the PPA group brains. Tubulin IIIβ (neuronal marker) was significantly decreased in the 5 M group. IL-6 and TNF-α expression were increased in the brain of the PPA group (IL-6: 2.48 ± 1.25-fold at 5 M; TNF-α: 2.84 ± 1.16-fold at 1 M and 2.64 ± 1.42-fold, at 5 M), while IL-10 was decreased. GPR41 and p-Akt were increased, while PTEN (p-Akt inhibitor) was decreased in the PPA group. The data support the role of a PPA-rich diet in glia over-proliferation and neuro-inflammation mediated by the GPR41 receptor and PTEN/Akt pathway. These findings strongly support our earlier study on the role of PPA in ASD. Full article
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Review

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23 pages, 977 KB  
Review
The Regulatory Role of FABP4 in Microbiome–Brain–Gut Communication Under High-Fat-Diet Conditions
by Katarzyna Smolińska, Ewa Tomaszewska, Monika Hułas-Stasiak, Siemowit Muszyński, Aleksandra Szopa, Anna Serefko and Piotr Dobrowolski
Int. J. Mol. Sci. 2026, 27(5), 2430; https://doi.org/10.3390/ijms27052430 - 6 Mar 2026
Viewed by 591
Abstract
High-fat diets (HFDs) are major environmental factors influencing metabolic homeostasis, immune regulation, and brain function, largely through their effects on gut microbiota and intestinal barrier integrity. Disruption of the microbiome–brain–gut axis has been increasingly implicated in systemic and neuroinflammatory processes; however, the molecular [...] Read more.
High-fat diets (HFDs) are major environmental factors influencing metabolic homeostasis, immune regulation, and brain function, largely through their effects on gut microbiota and intestinal barrier integrity. Disruption of the microbiome–brain–gut axis has been increasingly implicated in systemic and neuroinflammatory processes; however, the molecular mediators that integrate dietary lipid signals with microbial and host responses remain incompletely defined. This review synthesizes the current evidence on the role of fatty acid-binding protein 4 (FABP4) as an integrative node linking HFD-induced gut dysbiosis to systemic and central inflammatory signaling. We critically evaluated experimental and translational studies addressing HFD-driven alterations in gut microbiota composition, intestinal barrier function, and inflammatory pathways, with particular emphasis on FABP4-mediated mechanisms across epithelial, immune, and neural compartments. The available data indicate that FABP4 responds to dietary and microbiome-derived cues and contributes to coordinated metabolic and inflammatory responses, affecting both peripheral tissues and the central nervous system. These findings support a model in which FABP4 participates in diet-driven feedback loops that amplify gut barrier dysfunction, immune activation, and neuroinflammation. In conclusion, FABP4 emerges as a central molecular mediator within the microbiome–brain–gut axis under HFD conditions, highlighting its potential relevance in understanding the pathophysiology of metabolic and neuroinflammatory disorders and guiding future integrative research strategies. Full article
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