# Children’s gut microbiota predicts the efficacy of obesity treatment

**Authors:** Mireia Alcázar, Verónica Luque, Natalia Ferré, Judit Muñoz-Hernando, Mariona Gispert-Llauradó, Ricardo Closa-Monasterolo, Albert Feliu, Gemma Castillejo, Joaquín Escribano

PMC · DOI: 10.1080/19490976.2026.2631824 · Gut Microbes · 2026-02-19

## TL;DR

The study shows that children with a more diverse gut microbiome and certain bacteria respond better to obesity treatments.

## Contribution

It identifies specific gut microbiota signatures that predict treatment success in childhood obesity.

## Key findings

- Higher baseline gut microbiota diversity correlates with better metabolic improvements after one year.
- Faecalibacterium abundance is the most influential predictor of treatment success.
- A Simpson index cut-off of 0.849 can stratify children into high- and low-diversity groups with different treatment outcomes.

## Abstract

Responses to dietary interventions may vary depending on baseline gut microbiota composition. This study aimed to determine whether baseline gut microbiota diversity and composition predict the effectiveness of childhood obesity interventions.

Anthropometry, triglycerides, HDL-cholesterol, HOMA-IR, and systolic and diastolic blood pressure (SBP, DBP) were evaluated and standardised in 41 children with obesity (8–14yrs). Faecal samples were collected at baseline and after one year. Intervention success was defined by improvements in metabolic risk score (MetScore) or BMI z-score. Associations between baseline microbiota features (diversity and composition) and intervention success were evaluated using Spearman’s correlation and linear regression models. Gut microbiota composition and differential abundance were analyzed using ANCOM-BC2. Exploratory biomarker discovery was analyzed using LEfSe, and predictive modelling using a Random Forest (RF) classifier. Receiver operating characteristic (ROC) curve analysis was used to determine a Simpson index cut-off.

Higher baseline Shannon and Simpson indices, and greater abundances of Faecalibacterium and Eubacterium coprostanoligenes group, were associated with greater improvements in MetScore. Faecalibacterium was the most influential feature with the highest importance in the RF model, which achieved an AUC of 0.876 for MetScore and 0.873 for BMI z-score improvement. Eighty-four features differed between MetScore response groups (FDR < 0.05) with some genus-level overlap with the exploratory analysis, including Eubacterium coprostanoligenes and Ruminococcus. A Simpson index cut-off of 0.849 stratified participants high- and low-diversity groups; children above this threshold exhibited greater improvements in MetScore (p = 0.028), SBP (p = 0.043), and in HDL-cholesterol (p = 0.028).

Higher baseline gut microbiota diversity and specific microbial signatures, particularly Faecalibacterium abundance, predicted better outcomes in childhood obesity interventions. These findings support the potential use of microbiota profiling to guide personalised treatment strategies. Further research is needed to optimise interventions.

Trial registration: clinicaltrials.gov NCT03749291.

## Linked entities

- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}
- **Diseases:** hypothyroidism (MESH:D007037), inflammatory (MESH:D007249), cardiometabolic disorders (MESH:D024821), weight loss (MESH:D015431), anxiety (MESH:D001007), Insulin Resistance (MESH:D007333), Childhood and Adolescent Obesity (MESH:D063766), endocrine disorders (MESH:D004700), overweight (MESH:D050177), eating disorders (MESH:D001068), homeostasis (MESH:D008232), inflammatory bowel syndrome (MESH:D015212), Obesity (MESH:D009765), MetScore (MESH:D008659), growth hormone deficiency (MESH:D004393), precocious puberty (MESH:D011629), Cushing's syndrome (MESH:D003480)
- **Chemicals:** coprostanol (MESH:D004083), oligosaccharides (MESH:D009844), FODMAP (-), triglyceride (MESH:D014280), monosaccharides (MESH:D009005), carbohydrate (MESH:D002241), Butyrate (MESH:D002087), polyols (MESH:C024617), disaccharides (MESH:D004187), Glucose (MESH:D005947), cholesterol (MESH:D002784), SCFA (MESH:D005232)
- **Species:** Subdoligranulum (genus) [taxon 292632], Holdemanella (genus) [taxon 1573535], Faecalibacterium (genus) [taxon 216851], Akkermansia muciniphila (species) [taxon 239935], Haemophilus (genus) [taxon 724], Clostridium (genus) [taxon 1485], Eubacterium coprostanoligenes (species) [taxon 290054], Bifidobacterium (genus) [taxon 1678], Lactobacillus (genus) [taxon 1578], Homo sapiens (human, species) [taxon 9606], Faecalibacterium prausnitzii (species) [taxon 853], Bacteroides (genus) [taxon 816], Ruminococcus (genus) [taxon 1263], gut metagenome (species) [taxon 749906], Roseburia (genus) [taxon 841]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12928635/full.md

## References

52 references — full list in the complete paper: https://tomesphere.com/paper/PMC12928635/full.md

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Source: https://tomesphere.com/paper/PMC12928635