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Purpose of Review <p>The association of the gut microbiome with T2DM has been conflicting due to the disease’s inherent complexity—a challenge that is further exacerbated in T2DM-related atherosclerotic cardiovascular diseases (ASCVD). Even when individual microbial species are associated with T2DM or ASCVD, mechanisms remain elusive—highlighting a pressing need for gut microbiota profiling in T2DM-related ASCVD. This perspective review examines gut microbial dysbiosis in T2DM with atherosclerosis (T2DM-AS), focusing on population-specific profiles from southern China and microbial biomarkers to predict disease progression.</p> Recent Findings <p>T2DM-AS patients exhibit reduced Firmicutes-to-Bacteriodota ratio, with reduced Clostridia, Oscillospirales, Ruminococcaceae, and <i>Faecalibacterium</i>. Dysbiosis includes increased pro-inflammatory Enterobacteriaceae, Enterococcaceae, and Streptococcaceae, with higher abundances of <i>Escherichia-Shigella</i>, <i>Klebsiella</i>, <i>Streptococcus</i>, and <i>Alloprevotella</i>. Beneficial butyrate-producing genera <i>Faecalibacterium</i>, <i>Dialister</i>, and <i>Butyricicoccus</i> are markedly depleted. Enterobacteriaceae/<i>Escherichia-Shigella</i> abundance strongly correlates with the Gensini score, serum zonulin (a gut permeability marker), cholesterol, triglyceride, and alanine aminotransferase. Mechanistically, the bacterial type III secretion system primarily drives a pathogenic cascade involving: (1) ferroptosis-mediated intestinal damage, (2) gut barrier disruption, (3) abnormal glycerophospholipid metabolism with phosphatidylcholine upregulation, and (4) macrophage activation and systemic inflammation that aggravates atherosclerosis.</p> Summary <p>Pathogenic gut microbial signatures—enrichment of type III secretion system-harboring Enterobacteriaceae and depletion of butyrate-producing taxa—represent potential biomarkers for T2DM-AS progression. The type III secretion system-ferroptosis-lipid metabolism axis critically links gut dysbiosis to accelerated atherosclerosis, suggesting interventions targeting gut barrier integrity or lipid metabolism as therapeutic avenues. Population-specific profiling is essential for microbiome-based approaches to T2DM-AS management.</p>

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Gut Microbial Dysbiosis in Type 2 Diabetes Patients with Concurrent Atherosclerosis

  • 期刊论文

  • 发表日期：

    2026年5月21日

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  • Abdul Sammad,
  • Sohrab Khan,
  • Yao-Yuan Zhang,
  • Xin-Ling Bai,
  • Xiao Zhu,
  • Kai Yin

摘要

Purpose of Review

The association of the gut microbiome with T2DM has been conflicting due to the disease’s inherent complexity—a challenge that is further exacerbated in T2DM-related atherosclerotic cardiovascular diseases (ASCVD). Even when individual microbial species are associated with T2DM or ASCVD, mechanisms remain elusive—highlighting a pressing need for gut microbiota profiling in T2DM-related ASCVD. This perspective review examines gut microbial dysbiosis in T2DM with atherosclerosis (T2DM-AS), focusing on population-specific profiles from southern China and microbial biomarkers to predict disease progression.

Recent Findings

T2DM-AS patients exhibit reduced Firmicutes-to-Bacteriodota ratio, with reduced Clostridia, Oscillospirales, Ruminococcaceae, and Faecalibacterium. Dysbiosis includes increased pro-inflammatory Enterobacteriaceae, Enterococcaceae, and Streptococcaceae, with higher abundances of Escherichia-Shigella, Klebsiella, Streptococcus, and Alloprevotella. Beneficial butyrate-producing genera Faecalibacterium, Dialister, and Butyricicoccus are markedly depleted. Enterobacteriaceae/Escherichia-Shigella abundance strongly correlates with the Gensini score, serum zonulin (a gut permeability marker), cholesterol, triglyceride, and alanine aminotransferase. Mechanistically, the bacterial type III secretion system primarily drives a pathogenic cascade involving: (1) ferroptosis-mediated intestinal damage, (2) gut barrier disruption, (3) abnormal glycerophospholipid metabolism with phosphatidylcholine upregulation, and (4) macrophage activation and systemic inflammation that aggravates atherosclerosis.

Summary

Pathogenic gut microbial signatures—enrichment of type III secretion system-harboring Enterobacteriaceae and depletion of butyrate-producing taxa—represent potential biomarkers for T2DM-AS progression. The type III secretion system-ferroptosis-lipid metabolism axis critically links gut dysbiosis to accelerated atherosclerosis, suggesting interventions targeting gut barrier integrity or lipid metabolism as therapeutic avenues. Population-specific profiling is essential for microbiome-based approaches to T2DM-AS management.