AI Article Synopsis

  • Research shows a significant link between gut microbiota imbalances and the development of type 2 diabetes (T2D) and coronary artery disease (CAD), especially their connection in diabetic coronary artery disease (DCAD).
  • The study used Mendelian randomization to analyze genetic data and identify relationships between gut microbiota, T2D, and CAD, revealing a causal link where a genetic predisposition to T2D correlates with increased gut microbiota presence and a higher likelihood of CAD.
  • The findings suggest that T2D can raise CAD risk through gut microbiota changes, with specific metabolites like TMAO playing a crucial role, while also indicating that DCAD may influence gut microbiota composition.

Article Abstract

The current body of research points to a notable correlation between an imbalance in gut microbiota and the development of type 2 diabetes mellitus (T2D) as well as its consequential ailment, coronary artery disease (CAD). The complexities underlying the association, especially in the context of diabetic coronary artery disease (DCAD), are not yet fully understood, and the causal links require further clarification. In this study, a bidirectional Mendelian randomization (MR) methodology was utilized to explore the causal relationships between gut microbiota, T2D, and CAD. By analyzing data from the DIAGRAM, GERA, UKB, FHS, and mibioGen cohorts and examining GWAS databases, we sought to uncover genetic variants linked to T2D, CAD, and variations in gut microbiota and metabolites, aiming to shed light on the potential mechanisms connecting gut microbiota with DCAD. Our investigation uncovered a marked causal link between the presence of and an increased incidence of both T2D and CAD. Specifically, a ten-unit genetic predisposition towards T2D was found to be associated with a 6.1% higher probability of an increase in the family's presence (β = 0.061, 95% CI = 0.002-0.119). In a parallel finding, an augmented presence of was related to an 8.2% heightened genetic likelihood of CAD (β = 0.082, 95% CI = 0.026-0.137). This evidence indicates a critical pathway by which T2D can potentially raise the risk of CAD via alterations in gut microbiota. Additionally, our analyses reveal a connection between CAD risk and , thus providing fresh perspectives on the roles of TMAO and carnitine in the etiology of CAD. The data also suggest a direct causal relationship between increased levels of certain metabolites - , , , and - and the prevalence of both T2D and CAD. Sensitivity assessments reinforce the notion that changes in could pose a risk for DCAD. There is also evidence to suggest that DCAD may, in turn, affect the gut microbiota's makeup. Notably, a surge in serum TMAO levels in individuals with CAD, coinciding with a reduced presence of methanogens, has been identified as a potentially significant factor for future examination.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10758148PMC
http://dx.doi.org/10.7150/ijms.92131DOI Listing

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