# Amelioration of Metabolic Syndrome by Co-Administration of Lactobacillus johnsonii CRL1231 and Wheat Bran in Mice via Gut Microbiota and Metabolites Modulation

**Authors:** Matias Russo, Antonela Marquez, Estefanía Andrada, Sebastián Torres, Arlette Santacruz, Roxana Medina, Paola Gauffin-Cano

PMC · DOI: 10.3390/metabo15070466 · 2025-07-09

## TL;DR

Combining a specific Lactobacillus strain with wheat bran improves metabolic syndrome in mice by altering gut bacteria and metabolites.

## Contribution

The study demonstrates a synergistic dietary approach using Lactobacillus johnsonii and wheat bran to alleviate metabolic syndrome through gut microbiota and metabolite modulation.

## Key findings

- Co-administration of Lactobacillus johnsonii and wheat bran reduced adiposity and improved cholesterol levels in mice.
- The treatment increased beneficial gut bacteria and decreased harmful ones, while also reducing inflammation and liver damage.
- Colonic feruloyl esterase activity and FA-derived metabolites were elevated, contributing to metabolic improvements.

## Abstract

Background/Objectives: Lactobacillus johnsonii CRL1231 (Lj CRL1231) is a strain with feruloyl esterase (FE) activity that enhances ferulic acid (FA) release from wheat bran (WB) and has potential as a probiotic for metabolic syndrome (MS). Given the potential health benefits of FA and its microbial metabolites, this study aimed to evaluate the therapeutic effect of Lj CRL1231 co-administered with WB in a mouse model of metabolic syndrome (MS) induced by a high-fat diet (HFD). Methods: Mice were divided into three groups and fed for 14 weeks as follows: the Control group (standard diet), the MS group (HFD+WB), and the MS+Lj group (HFD+WB and Lj CRL1231-dose 108 cells/day). Specifically, we analyzed the changes in the intestinal microbiota (IM), colonic FE activity, generation of FA-derived and fermentation metabolites, and metabolic and inflammatory parameters. Results: Improvements in the MS+Lj group compared to the MS group included the following: a—a 38% increase in colonic FE activity, leading to elevated levels of FA-derived metabolites (e.g., dihydroferulic, dihydroxyphenylpropionic, and hydroxyphenylpropionic acids); b—a significant shift in the IM composition, with a 3.4-fold decrease in Firmicutes and a 2.9-fold increase in Bacteroidetes; c—a decrease in harmful bacteria (Desulfovibrio) by 93%, and beneficial bacteria like Bifidobacterium increased significantly (6.58 log cells/g); d—a 33% increase in total SCFAs; e—a 26% reduction in the adiposity index; f—a 12% increase in HDL cholesterol and a 19% reduction in triglycerides; g—normalized glucose and insulin resulting in a 2-fold lower HOMA-IR index; h—an improved inflammatory profile by decreasing TNF-α, IFN-γ, and IL-6 (3-, 5-, and 2-fold, respectively) and increasing IL-10 by 2-fold; i—alleviation of liver damage by normalizing of transaminases AST (19.70 ± 2.97 U/L) and ALT (13.12 ± 0.88 U/L); j—evidence of reduced oxidative damage. Conclusions: The co-administration of L. johnsonii CRL1231 and WB exerts a synergistic effect in mitigating the features of MS in HFD-fed mice. This effect is mediated by modulation of the gut microbiota, increased release of bioactive FA-derived compounds, and restoration of metabolic and inflammatory homeostasis. This strategy represents a promising dietary approach for MS management through targeted microbiota–metabolite interactions.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor), IFNG (interferon gamma), IL6 (interleukin 6), IL10 (interleukin 10), GOT1 (glutamic-oxaloacetic transaminase 1), GPT (glutamic--pyruvic transaminase)
- **Chemicals:** ferulic acid (PubChem CID 445858), dihydroferulic acid (PubChem CID 14340), hydroxyphenylpropionic acid (PubChem CID 1303)
- **Diseases:** metabolic syndrome (MONDO:0000816)
- **Species:** Desulfovibrio (taxon 872), Bifidobacterium (taxon 1678)

## Full-text entities

- **Genes:** Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, Il10 (interleukin 10) [NCBI Gene 16153] {aka CSIF, If2a, Il-10}, Ifng (interferon gamma) [NCBI Gene 15978] {aka IFN-g, If2f, Ifg}, Slc17a5 (solute carrier family 17 (anion/sugar transporter), member 5) [NCBI Gene 235504] {aka 4631416G20Rik, 4732491M05, AST, ISSD, NSD, SD}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}
- **Diseases:** inflammatory (MESH:D007249), liver damage (MESH:D056486), MS (MESH:D024821)
- **Chemicals:** cholesterol (MESH:D002784), triglycerides (MESH:D014280), glucose (MESH:D005947), FA (MESH:C004999), SCFAs (MESH:D005232), fat (MESH:D005223), Bran (-)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Desulfovibrio (genus) [taxon 872]

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12299901/full.md

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Source: https://tomesphere.com/paper/PMC12299901