1‐Piperideine as an In Vivo Precursor of the γ‐Aminobutyric Acid Homologue 5‐Aminopentanoic Acid

Callery, Patrick S.; Geelhaar, Linda A.

doi:10.1111/j.1471-4159.1985.tb04085.x

Cited by 18 publications

(13 citation statements)

References 14 publications

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“…Butyrate is important to intestinal barrier integrity. In addition, both 5-aminovalerate and butyrate can be produced by microbial metabolism of essential amino acid lysine [ 18 , 19 , 20 ]. The lack of T-cells also resulted in lower amounts of cecal ornithine at P28 (r = −0.537) and higher amounts of glucose-6-phosphate at 84 days (r = 0.513), metabolites related to amino acid metabolism and glycolysis.…”

Section: Resultsmentioning

confidence: 99%

Microbe-Immune Crosstalk: Evidence That T Cells Influence the Development of the Brain Metabolome

Caspani

Green

Swann

et al. 2022

IJMS

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Cross-talk between the immune system and the brain is essential to neuronal development, neuronal excitability, neuroplasticity, and neurotransmission. Gut microbiota are essential to immune system development and immune function; hence, it is essential to consider more broadly the microbiota-immune-brain axis in neurodevelopment. The gut, brain, and microbial metabolomes obtained from C57Bl/6 and T-cell-deficient mice across four developmental timepoints (postnatal day 17, 24, 28, and 84) were studied by 1H NMR spectroscopy. 16S rRNA gene sequencing was performed on cecal and fecal samples. In the absence of T-cells, the developmental trajectory of the gut microbiota and of the host’s metabolic profile was altered. The novel insights from this work include (1) the requirement of functional T-cells for the normal trajectory of microbiotal development and the metabolic maturation of the supra-organism, (2) the potential role for Muribaculaceae taxa in modulating the cecal availability of metabolites previously implicated with a role in the gut-brain axis in T-cell deficient mice, and (3) the impact of T-cell-deficiency on central levels of neuroactive metabolites.

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Section: Resultsmentioning

confidence: 99%

Microbe-Immune Crosstalk: Evidence That T Cells Influence the Development of the Brain Metabolome

Caspani

Green

Swann

et al. 2022

IJMS

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“…This metabolite can be produced both endogenously and through the bacterial catabolism of lysine. It is believed to act as a methylene homologue of γ-aminobutyric acid (GABA) and functions as a weak GABA agonist (Callery and Geelhaar 1985). Interestingly, GABA was also higher in the autistic models compared with the non-autistic models pre-treatment but these differences were not present following B-GOS treatment.…”

Section: Discussionmentioning

confidence: 99%

In vitrofermentation of B-GOS: impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children

Grimaldi

Cela

Swann

et al. 2016

FEMS Microbiology Ecology

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Children with autism spectrum disorders (ASD) often suffer gastrointestinal problems consistent with imbalances in the gut microbial population. Treatment with antibiotics or pro/prebiotics has been postulated to regulate microbiota and improve gut symptoms, but there is a lack of evidence for such approaches, especially for prebiotics. This study assessed the influence of a prebiotic galactooligosaccharide (B-GOS) on gut microbial ecology and metabolic function using faecal samples from autistic and non-autistic children in an in vitro gut model system. Bacteriology was analysed using flow cytometry combined with fluorescence in situ hybridization and metabolic activity by HPLC and 1H-NMR. Consistent with previous studies, the microbiota of children with ASD contained a higher number of Clostridium spp. and a lower number of bifidobacteria compared with non-autistic children. B-GOS administration significantly increased bifidobacterial populations in each compartment of the models, both with autistic and non-autistic-derived samples, and lactobacilli in the final vessel of non-autistic models. In addition, changes in other bacterial population have been seen in particular for Clostridium, Rosburia, Bacteroides, Atopobium, Faecalibacterium prausnitzii, Sutterella spp. and Veillonellaceae. Furthermore, the addition of B-GOS to the models significantly altered short-chain fatty acid production in both groups, and increased ethanol and lactate in autistic children.

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“…Although monoamine deficiency is the most frequently mentioned hypothesis for mood disorders, more recent evidence suggests that the glutamatergic system is also involved in the etiology. 53 , 54 The free acid form of 5-aminovaleric acid lactam, one of two metabolites whose levels were significantly affected in both plasma and CSF, is a gamma-aminobutyric acid (GABA) homolog and has been shown to be a weak GABA agonist, 55 further implicating the glutamatergic system. We have preliminary data from mice that indicate that SSRI treatment results in altered glutamate levels in the hippocampus (Park et al , unpublished).…”

Section: Discussionmentioning

confidence: 99%

Identifying individual differences of fluoxetine response in juvenile rhesus monkeys by metabolite profiling

Hogrefe

Palazoglu

et al. 2014

Transl Psychiatry

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Fluoxetine is the only psychopharmacological agent approved for depression by the US Food and Drug Administration for children and is commonly used therapeutically in a variety of neurodevelopmental disorders. Therapeutic response shows high individual variability, and severe side effects have been observed. In the current study we set out to identify biomarkers of response to fluoxetine as well as biomarkers that correlate with impulsivity, a measure of reward delay behavior and potential side effect of the drug, in juvenile male rhesus monkeys. The study group was also genotyped for polymorphisms of monoamine oxidase A (MAOA), a gene that has been associated with psychiatric disorders. We used peripheral metabolite profiling of blood and cerebrospinal fluid (CSF) from animals treated daily with fluoxetine or vehicle for one year. Fluoxetine response metabolite profiles and metabolite/reward delay behavior associations were evaluated using multivariate analysis. Our analyses identified a set of plasma and CSF metabolites that distinguish fluoxetine- from vehicle-treated animals and metabolites that correlate with impulsivity. Some metabolites displayed an interaction between fluoxetine and MAOA genotype. The identified metabolite biomarkers belong to pathways that have important functions in central nervous system physiology. Biomarkers of response to fluoxetine in the normally functioning brain of juvenile nonhuman primates may aid in finding predictors of response to treatment in young psychiatric populations and in progress toward the realization of a precision medicine approach in the area of neurodevelopmental disorders.

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1‐Piperideine as an In Vivo Precursor of the γ‐Aminobutyric Acid Homologue 5‐Aminopentanoic Acid

Cited by 18 publications

References 14 publications

Microbe-Immune Crosstalk: Evidence That T Cells Influence the Development of the Brain Metabolome

Microbe-Immune Crosstalk: Evidence That T Cells Influence the Development of the Brain Metabolome

In vitrofermentation of B-GOS: impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children

Identifying individual differences of fluoxetine response in juvenile rhesus monkeys by metabolite profiling

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