Home Research Feeds Gastrointestinal Autonomic Neuropathy Exacerbates Gut Microbiota Dysbiosis in Adult Patients With Type 2 Diabetes Mellitus

Gastrointestinal Autonomic Neuropathy Exacerbates Gut Microbiota Dysbiosis in Adult Patients With Type 2 Diabetes MellitusOriginal paper

Researched by:

  • Karen Pendergrass

Last Updated: 2026-07-05

Karen Pendergrass
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.

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Location
China
Sample Site
Feces
Species
Homo sapiens

What was studied?

This study compared gut microbiota among healthy adults, patients with type 2 diabetes, and patients with type 2 diabetes plus gastrointestinal autonomic neuropathy. It asked whether neuropathy deepens microbial dysbiosis. DNA from fecal samples was sequenced across the 16S rRNA gene V4 region on the Illumina MiSeq platform. The team measured diversity, composition at multiple taxonomic levels, and predicted functions with PICRUSt2. LEfSe identified biomarker taxa, and Spearman analysis linked taxa to clinical data.

Who was studied?

Participants were adults recruited in Kunming, China: 19 healthy controls, 73 patients with type 2 diabetes, and 27 with type 2 diabetes plus gastrointestinal autonomic neuropathy who completed the trial. All patients met WHO diagnostic criteria for type 2 diabetes, and all with neuropathy had diabetes for over 3 years. Patients with neuropathy were older and had lower body mass index and triglycerides than diabetes patients without it. Controls were age- and sex-matched.

What were the most important findings?

Neuropathy worsened dysbiosis, and the sharpest differences came from the phyla Fusobacteria and Proteobacteria. Bacteroidetes fell progressively from controls to diabetes to neuropathy patients (65.19% versus 59.13% versus 52.56%). Fusobacteria was significantly higher in diabetes than in neuropathy patients (p=0.011). Diabetes patients were characterized by phylum Fusobacteria, class Fusobacteriia, and family Fusobacteriaceae. Neuropathy patients were characterized by class Gammaproteobacteria, order Enterobacteriales, and family Enterobacteriaceae. Their microbes linked to bacterial invasion of epithelial cells and pathogenic infection pathways.

What are the greatest implications of this study?

The findings suggest gut dysbiosis tracks with diabetes progression and its gastrointestinal complications. Gammaproteobacteria, a source of lipopolysaccharide, may promote the neuropathy state. This points to microbiota-targeted options such as probiotics or prebiotics as possible tools to prevent or manage complications. Groups differed in age and body mass index, controls lacked full clinical data, and functions were only predicted, so causation cannot be inferred.

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