The Vitamin B6 and Gut-brain Interplay: Investigating the Role of Vitamin B6 in Regulating Gut Microbiome, Metabolites and Behaviour Using a Rodent Model

Monday, Oct. 27, 1-2 p.m.

CSF-1302

The direct link for the meeting is:

https://mun.webex.com/mun/j.php?MTID=m8eb8fa64bff11dc99b8a3b57ab31a2ac

Abstract

Vitamin B6 (VB6) plays a critical role in several metabolic pathways, including one-carbon metabolism and neurotransmitter synthesis, yet its impact on gut-brain communication remains underexplored. Emerging evidence suggests that B vitamin deficiencies can disturb the gut microbiome. Furthermore, VB6-induced gut dysbiosis alters the production of intestinal short-chain fatty acids (SCFAs) and neuroactive metabolites, which may influence not only the gut-brain axis but also the gut-liver axis. Hence, this research examined how VB6 deficiency influences gut microbiota, microbial metabolites, and neurobehavioral outcomes in both healthy and disease animal models.

First, we investigated the impact of dietary VB6 on gut homeostasis and behavioural outcomes using Sprague-Dawley rats. VB6 deficiency led to significant reductions in plasma VB6, brain gamma-aminobutyric acid, and increased glutamic acid, and anxiety-like behaviors. Alterations in gut microbiota were also observed, including increased abundances of Lachnospiraceae sp., Mucispirillum schaedleri, and Harryflintia sp. and a decrease in Muribaculaceae sp., Bacteroides vulgatus, and Bilophila sp. Microbial metabolites such as SCFA levels, particularly propionate and isobutyrate, declined, correlating with behavioural and neurochemical changes. We further investigated the impact of VB6 in an animal model of metabolic disease. C57BL/6J mice were fed with a high-fat, high-sugar (HFHS) diet for 8 weeks to induce Metabolic dysfunction-associated Steatotic Liver Disease (MASLD) along with varying levels of dietary VB6. HFHS diet altered gut microbiota diversity and composition, increasing the abundance of the phyla Firmicutes and Verrucomicrobiota while decreasing the Bacteroidota and Actinobacteria. The VB6 deficiency further modulated the gut microbiome at the species level. This has also led to a reduction in cecal SCFAs, including acetate. The brain cortex metabolites analyzed by untargeted metabolomics were distinctly altered.

Together, these findings suggest VB-6 deficiency disrupts gut microbial balance and SCFA production, leading to neurochemical and behavioral alterations via the gut–brain axis. This highlights the importance of VB-6 in maintaining gut-brain communication and may inform therapeutic strategies for metabolic and neurological disorders.

Thank you,

Presented by Department of Biochemistry

Event Listing 2025-10-27 13:00:00 2025-10-27 14:00:00 America/St_Johns The Vitamin B6 and Gut-brain Interplay: Investigating the Role of Vitamin B6 in Regulating Gut Microbiome, Metabolites and Behaviour Using a Rodent Model The direct link for the meeting is: https://mun.webex.com/mun/j.php?MTID=m8eb8fa64bff11dc99b8a3b57ab31a2ac Abstract Vitamin B6 (VB6) plays a critical role in several metabolic pathways, including one-carbon metabolism and neurotransmitter synthesis, yet its impact on gut-brain communication remains underexplored. Emerging evidence suggests that B vitamin deficiencies can disturb the gut microbiome. Furthermore, VB6-induced gut dysbiosis alters the production of intestinal short-chain fatty acids (SCFAs) and neuroactive metabolites, which may influence not only the gut-brain axis but also the gut-liver axis. Hence, this research examined how VB6 deficiency influences gut microbiota, microbial metabolites, and neurobehavioral outcomes in both healthy and disease animal models. First, we investigated the impact of dietary VB6 on gut homeostasis and behavioural outcomes using Sprague-Dawley rats. VB6 deficiency led to significant reductions in plasma VB6, brain gamma-aminobutyric acid, and increased glutamic acid, and anxiety-like behaviors. Alterations in gut microbiota were also observed, including increased abundances of Lachnospiraceae sp., Mucispirillum schaedleri, and Harryflintia sp. and a decrease in Muribaculaceae sp., Bacteroides vulgatus, and Bilophila sp. Microbial metabolites such as SCFA levels, particularly propionate and isobutyrate, declined, correlating with behavioural and neurochemical changes. We further investigated the impact of VB6 in an animal model of metabolic disease. C57BL/6J mice were fed with a high-fat, high-sugar (HFHS) diet for 8 weeks to induce Metabolic dysfunction-associated Steatotic Liver Disease (MASLD) along with varying levels of dietary VB6. HFHS diet altered gut microbiota diversity and composition, increasing the abundance of the phyla Firmicutes and Verrucomicrobiota while decreasing the Bacteroidota and Actinobacteria. The VB6 deficiency further modulated the gut microbiome at the species level. This has also led to a reduction in cecal SCFAs, including acetate. The brain cortex metabolites analyzed by untargeted metabolomics were distinctly altered. Together, these findings suggest VB-6 deficiency disrupts gut microbial balance and SCFA production, leading to neurochemical and behavioral alterations via the gut–brain axis. This highlights the importance of VB-6 in maintaining gut-brain communication and may inform therapeutic strategies for metabolic and neurological disorders. Thank you, CSF-1302 Department of Biochemistry