Imbalance of Fecal Microbiota at Newly Diagnosed Type 1 Diabetes in Chinese Children Original paper
Researched by:
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Dr. Umar
ID
Dr. Umar
Read MoreClinical 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.
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Dr. Umar
Read More
Researched by:
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Dr. Umar
ID
Dr. Umar
Read More
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
Location
China
Sample Site
Feces
Species
Homo sapiens
What was studied?
This case-control study examined t1dm-gut-microbiota-signatures by comparing fecal bacterial community structure in Chinese children with newly diagnosed type 1 diabetes (T1DM) versus matched healthy controls, using high-throughput 16S rDNA sequencing and community metrics (including Chao richness) alongside clustering and biomarker-discovery analyses (PCoA/UniFrac, LEfSe).
Who was studied?
Thirty Chinese children were enrolled at Peking Union Medical College Hospital (Beijing) from September 2014 to June 2015: 15 newly diagnosed T1DM cases (<6 months; ada criteria plus ≥1 persistent islet autoantibody) and 15 autoantibody-negative healthy controls matched for age, sex, race, delivery mode, breastfeeding duration. exclusions minimized confounding from infections inflammatory disease, gi disorders, recent antibiotics pro- prebiotics (within 3 months). < p>
Most important findings
Children with T1DM showed a measurable ecological shift characterized by lower fecal bacterial richness (Chao index) compared with controls, while overall diversity (Shannon) was not significantly different, suggesting fewer distinct taxa rather than a uniformly “less even” community. The global community structure also separated between groups on unweighted UniFrac PCoA, consistent with a disease-associated compositional reorganization. At broad taxonomic levels, dominant phyla (Bacteroidetes and Firmicutes) did not differ significantly, indicating that the key discriminatory signal sat deeper—at order/family/genus/species resolution. LEfSe and nonparametric testing highlighted an increase in Blautia in T1DM and reductions in several taxa often nested within Firmicutes or Proteobacteria-related lineages, including Haemophilus, Lachnospira, Dialister, Acidaminococcus, and Intestinimonas (plus Pasteurellales/Pasteurellaceae and Caulobacterales). Clinically, Blautia abundance correlated positively with glycemic control burden (HbA1c) and autoimmune activity (number of T1DM autoantibodies and IA-2 titers), linking a specific genus-level shift to both metabolic and immune phenotypes and making Blautia a high-priority candidate feature for a microbiome signatures database in early T1DM.
| Microbial feature | Direction/clinical link |
|---|---|
| Community richness (Chao) | Lower in T1DM vs controls |
| Blautia (genus) | Higher in T1DM; positively correlated with HbA1c and autoantibody burden (incl. IA-2) |
| Intestinimonas (species) and Lachnospira/Dialister (genera) | Lower in T1DM; collectively suggest loss of potentially beneficial fermenters (incl. butyrate-related capacity) |
Key implications
This paper supports the idea that early T1DM in children is accompanied by a genus-/species-level dysbiosis rather than a simple phylum-level shift, and it ties at least one taxon (Blautia) to clinically meaningful immune and glycemic markers. For clinicians and microbiome translation, the practical takeaway is hypothesis-generating (not practice-changing): newly diagnosed pediatric T1DM may have reproducible fecal features that could inform risk stratification, mechanistic studies of gut permeability/immune education, and future microbiota-modulating adjuncts—while the small, single-region sample and cross-sectional design limit causality and generalizability.
Citation
Qi CJ, Zhang Q, Yu M, Xu JP, Zheng J, Wang T, Xiao XH. Imbalance of Fecal Microbiota at Newly Diagnosed Type 1 Diabetes in Chinese Children. Chin Med J. 2016;129(11):1298-1304. doi:10.4103/0366-6999.182841
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.