Fecal microbiota imbalance in Mexican children with type 1 diabetes Original paper

Researched by:

  • Dr. Umar ID
    Dr. Umar

    User avatarClinical Pharmacist and Clinical Pharmacy Master’s candidate focused on antibiotic stewardship, AI-driven pharmacy practice, and research that strengthens safe and effective medication use. Experience spans digital health research with Bloomsbury Health (London), pharmacovigilance in patient support programs, and behavioral approaches to mental health care. Published work includes studies on antibiotic use and awareness, AI applications in medicine, postpartum depression management, and patient safety reporting. Developer of an AI-based clinical decision support system designed to enhance antimicrobial stewardship and optimize therapeutic outcomes.

    Read More

January 16, 2026

Researched by:

  • Dr. Umar ID
    Dr. Umar

    User avatarClinical Pharmacist and Clinical Pharmacy Master’s candidate focused on antibiotic stewardship, AI-driven pharmacy practice, and research that strengthens safe and effective medication use. Experience spans digital health research with Bloomsbury Health (London), pharmacovigilance in patient support programs, and behavioral approaches to mental health care. Published work includes studies on antibiotic use and awareness, AI applications in medicine, postpartum depression management, and patient safety reporting. Developer of an AI-based clinical decision support system designed to enhance antimicrobial stewardship and optimize therapeutic outcomes.

    Read More

Last Updated: 2014-01-01

Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

Location
Mexico
Sample Site
Feces
Species
Homo sapiens

What was studied?

This study characterized the Mexican-children-type-1-diabetes-gut-microbiome signature by comparing fecal bacterial community structure in pediatric type 1 diabetes (T1D) at diagnosis versus longer-term insulin-treated T1D and healthy controls. Using 16S rRNA (V4) amplicon sequencing (454 pyrosequencing) plus HLA risk haplotyping and clinical-history capture, the investigators asked whether T1D status and disease stage aligned with reproducible genus-level shifts rather than broad phylum changes, and whether insulin treatment corresponded to partial “normalization” of the community profile.

Who was studied?

The cohort comprised 29 Sonoran (northwest Mexico), predominantly “mestizo” children aged 7–18 years: 8 newly diagnosed T1D cases (<2 months duration), 13 established t1d cases on insulin for ≥2 years with hba1c <8%, and 8 healthy controls (including 4 siblings of cases). all participants were antibiotic-free at least 3 before stool collection; notably, reported antibiotic treatment frequency in the year(s) diagnosis was higher than controls, a relevant exposure when interpreting microbiome differences. genetically predisposed: nearly carried one hla risk allele, high prevalence drb104 (DR4) and DRB103 (DR3) variants.

Most important findings

Overall alpha diversity (within-sample diversity) did not differ significantly across groups, but beta diversity showed that newly diagnosed T1D cases clustered apart from controls, indicating a distinct community structure at disease onset. The separation was driven primarily at the genus level: controls exhibited a Prevotella-dominant profile, whereas new-onset T1D showed significantly higher Bacteroides and reduced Prevotella, with additional depletion of Megamonas and Acidaminococcus. Children treated for ≥2 years displayed intermediate abundances, suggesting partial movement toward the control-like (Prevotella-richer) state with insulin treatment, though treated individuals were more heterogeneous and did not form a tight cluster. Importantly for a microbiome signatures database, the discriminating signal here is best summarized as a Prevotella-dominant (control) versus Bacteroides-enriched (new-onset T1D) enterotype-like pattern, without a significant Bacteroidetes/Firmicutes ratio difference, emphasizing that genus-level directionality is the clinically salient layer.

Microbial feature (genus)Association in T1D vs controls
BacteroidesEnriched in new-onset T1D (significant)
PrevotellaDepleted in new-onset T1D; dominant in controls (significant)
MegamonasReduced in new-onset T1D (significant)

Key implications

Clinically, these data support the idea that pediatric T1D—especially at onset—correlates with a fecal microbiome configuration consistent with impaired mucosal barrier support (Prevotella-poor) and increased representation of taxa (Bacteroides) hypothesized to influence mucus dynamics and gut permeability pathways, but the cross-sectional design cannot establish causality. For translation, the most usable “signature” is the onset-specific shift toward Bacteroides enrichment with concomitant Prevotella depletion, while insulin-treated patients may partially revert yet remain variable—highlighting stage, recent antibiotic history, and diet as essential covariates when interpreting microbiome biomarkers or designing interventions.

Citation

Mejía-León ME, Petrosino JF, Ajami NJ, Domínguez-Bello MG, Calderón de la Barca AM. Fecal microbiota imbalance in Mexican children with type 1 diabetes. Sci Rep. 2014;4:3814. doi:10.1038/srep03814

Diabetes Type I

Type 1 diabetes is an autoimmune condition in which pancreatic β-cells are destroyed, causing insulin deficiency and hyperglycemia. It typically arises in youth and requires lifelong insulin therapy. This article provides a clinician-focused review of T1D’s causes, mechanisms, complications, diagnosis, and management, including emerging multi-omics insights.

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