Gut-brain axis: beneficial impact of Shouchella clausii spores on fructose induced dysfunction is associated with modulation of the deoxycholic acid - TGR5 pathway.
Overview
- Institute for the Animal Production System in the Mediterranean Environment, National Research Council, P.Le Enrico Fermi 1, Portici, 80055 Italy
- Department of Biology, University of Naples Federico II, Complesso Universitario Monte S. Angelo, Edificio 7, Via Cintia, Naples, 80126 Italy
- Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, Via Pansini 5, Naples, 80100 Italy
- NBFC, National Biodiversity Future Center, Palermo, 90133 Italy
- Task Force On Microbiome Studies, University of Naples Federico II, Naples, 80126 Italy
Abstract
Objective: The increased intake of added sweeteners, such as high-fructose corn syrup, has been associated with a rise in metabolic dysfunctions in gut and brain. While different evidence showed that dietary fructose induces gut microbiota reshaping, the sugar impact on specific bacteria-derived metabolites remains an understudied topic. In this study, we identified secondary bile acids (sBAs) as molecules differentially represented in plasma of rats fed a fructose-rich diet compared to control animals, and hypothesized that these metabolites might be a target for probiotic-based strategies to counteract sugar-induced metabolic disorders. To this aim, we investigated whether probiotic spores of Shouchella clausii SF174 ameliorate fructose-induced cognitive and metabolic dysfunctions and prevent molecular alterations in hippocampus and frontal cortex.
Methods: Wistar rats were fed a fructose-rich diet, alone or in combination with the daily administration of Shouchella clausii spores, for six weeks. At the end of treatment, behavioral, metabolomic and molecular analyses were performed.
Results: The probiotic spores exerted a protective effect on the memory function of fructose fed rats and prevented the decrease of markers of synaptic plasticity. This was associated with the maintenance of plasma and brain levels of the sBA deoxycholic acid and of its specific receptor Takeda G protein-coupled receptor 5. Further, spores beneficial modulation of fructose-induced peripheral and central inflammation was observed. Also, probiotic spores produced reshaping of the gut microbiota towards a composition exerting neuroprotective and anti-inflammatory effects.
Conclusion: These results suggest that sBAs might act as a communication bridge along the microbiota gut-brain axis and suggest that their modulation, through probiotic administration, represents an effective strategy to counteract fructose-induced neuroinflammation and gut-brain dysfunction.
Supplementary Information: The online version contains supplementary material available at 10.1186/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- bioproject:PRJNA1291627, at NCBI BioProject; found in the text, “DNA extraction, high-throughput sequencing and…”
Data availability
The data used and/
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 28 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 15 authors, 8 keywords, 13 MeSH terms, 3 funders, 84 references.
Cite
This paper
Spagnuolo, M. S., Petecca, N., De Palma, F., Troise, A. D., Di Porzio, A., Barrella, V., Saggese, A., De Pascale, S., De Stefano, M., Scaloni, A., Baccigalupi, L., Ricca, E., Iossa, S., Mazzoli, A., & Cigliano, L. (2026). Gut-brain axis: beneficial impact of Shouchella clausii spores on fructose induced dysfunction is associated with modulation of the deoxycholic acid - TGR5 pathway. Molecular medicine (Cambridge, Mass.), 32(1), 101. https://
BibTeX
@article{spagnuolo2026gu
author = {Spagnuolo, Maria Stefania and Petecca, Natasha and De Palma, Francesca and Troise, Antonio Dario and Di Porzio, Angela and Barrella, Valentina and Saggese, Anella and De Pascale, Sabrina and De Stefano, Marina and Scaloni, Andrea and Baccigalupi, Loredana and Ricca, Ezio and Iossa, Susanna and Mazzoli, Arianna and Cigliano, Luisa},
title = {{Gut-brain axis: beneficial impact of Shouchella clausii spores on fructose induced dysfunction is associated with modulation of the deoxycholic acid - TGR5 pathway}},
journal = {Molecular medicine (Cambridge, Mass.)},
year = {2026},
month = may,
volume = {32},
number = {1},
pages = {101},
publisher = {The Feinstein Institute for Medical Research},
issn = {1076-1551},
doi = {10.1186/
url = {https://
pmid = {42106599},
pmcid = {PMC13326143}
}
RIS
TY - JOUR
AU - Spagnuolo, Maria Stefania
AU - Petecca, Natasha
AU - De Palma, Francesca
AU - Troise, Antonio Dario
AU - Di Porzio, Angela
AU - Barrella, Valentina
AU - Saggese, Anella
AU - De Pascale, Sabrina
AU - De Stefano, Marina
AU - Scaloni, Andrea
AU - Baccigalupi, Loredana
AU - Ricca, Ezio
AU - Iossa, Susanna
AU - Mazzoli, Arianna
AU - Cigliano, Luisa
TI - Gut-brain axis: beneficial impact of Shouchella clausii spores on fructose induced dysfunction is associated with modulation of the deoxycholic acid - TGR5 pathway
T2 - Molecular medicine (Cambridge, Mass.)
J2 - Mol Med
PY - 2026
DA - 2026/
VL - 32
IS - 1
SP - 101
SN - 1076-1551
PB - The Feinstein Institute for Medical Research
DO - 10.1186/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1186/
"type": "article-journal",
"title": "Gut-brain axis: beneficial impact of Shouchella clausii spores on fructose induced dysfunction is associated with modulation of the deoxycholic acid - TGR5 pathway",
"container-title": "Molecular medicine (Cambridge, Mass.)",
"author": [
{
"family": "Spagnuolo",
"given": "Maria Stefania"
},
{
"family": "Petecca",
"given": "Natasha"
},
{
"family": "De Palma",
"given": "Francesca"
},
{
"family": "Troise",
"given": "Antonio Dario"
},
{
"family": "Di Porzio",
"given": "Angela"
},
{
"family": "Barrella",
"given": "Valentina"
},
{
"family": "Saggese",
"given": "Anella"
},
{
"family": "De Pascale",
"given": "Sabrina"
},
{
"family": "De Stefano",
"given": "Marina"
},
{
"family": "Scaloni",
"given": "Andrea"
},
{
"family": "Baccigalupi",
"given": "Loredana"
},
{
"family": "Ricca",
"given": "Ezio"
},
{
"family": "Iossa",
"given": "Susanna"
},
{
"family": "Mazzoli",
"given": "Arianna"
},
{
"family": "Cigliano",
"given": "Luisa"
}
],
"container-title-short":
"volume": "32",
"issue": "1",
"page": "101",
"DOI": "10.1186/
"PMID": "42106599",
"PMCID": "PMC13326143",
"ISSN": "1076-1551",
"publisher": "The Feinstein Institute for Medical Research",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
5,
9
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1186/s12974-026-03898-w
- TGR5 is essential for protecting from chronic stress-induced learning and memory impairments in mice by modulating inflammation associated with the gut-brain axis.Journal: Journal of neuroinflammationIn common: cellular / molecular, 3 references
- [2] doi:10.1007/s00429-026-03102-y
- Selective alterations in CA1 spine morphology following dietary fructose intake.Journal: Brain structure & functionIn common: rat, cellular / molecular, 2 references
- [3] doi:10.1016/j.redox.2026.104253
- Ursodeoxycholic acid mitigates cerebral ischemia/
reperfusion injury by inhibiting thrombin-induced lipid peroxidation through activation of ALDH3A1. Journal: Redox biologyIn common: cellular / molecular, 2 references - [4] doi:10.1080/17590914.2026.2696821
- Hijacking Sodium-Glucose Cotransporters: Fructose Drives Neuronal and Microglial Dysfunction.Journal: ASN neuroIn common: cellular / molecular, 2 references
- [5] doi:10.1371/journal.pone.0353463 [code]
- Distinct gut and oral microbiome patterns associated with dyslexia in a family-based cohort: A preliminary exploratory study.Journal: PloS oneIn common: 2 references
- [6] doi:10.1007/s10827-026-00935-8 [code]
- A biophysically grounded model of glutamatergic synaptic transmission integrating glutamate transport, receptor kinetics, and electrotonic effects.Journal: Journal of computational neuroscienceIn common: rat, cellular / molecular, 1 reference
- [7] doi:10.1186/s12916-026-04727-w
- Hypothesis-free evaluation of circulating metabolome provides cell-specific insights regarding the role of energy substrate availability in amyotrophic lateral sclerosis.Journal: BMC medicineIn common: cellular / molecular, 1 reference
- [8] doi:10.3389/frmbi.2026.1834726 [code]
- Shotgun metagenomic analysis reveals taxonomic and functional alterations in the gut microbiome across prodromal and symptomatic Lewy body disease.Journal: Frontiers in microbiomesIn common: cellular / molecular, 1 reference
- [9] doi:10.3389/fcimb.2026.1806356
- Global research trends in enteric nervous system and gut microbiota: a bibliometric analysis (2005-2025).Journal: Frontiers in cellular and infection microbiologyIn common: cellular / molecular, 1 reference
- [10] doi:10.3389/fnagi.2026.1839445 [code]
- The molecular mechanisms of Guizhi Fuling Pills in ameliorating Alzheimer's disease-like cognitive impairment: insights from transcriptomics, metabolomics, and gut microbiome.Journal: Frontiers in aging neuroscienceIn common: cellular / molecular, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.
