Related Experiment Video
Updated: May 5, 2026
05:28
Analysis of Fecal Microbiota Dynamics in Lupus-Prone Mice Using a Simple, Cost-Effective DNA Isolation Method
Published on: May 2, 2022
2.1K
Causal relationship between gut microbiota and diabetic nephropathy: a two-sample Mendelian randomization study.
Shuxiang Yan1, Hua Wang2,3, Baiyu Feng1
1Department of Nephrology, Hunan Key Laboratory of Kidney Disease and Blood Purification, Institute of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, China.
Frontiers in Immunology
|March 27, 2024
Summary
This study used Mendelian randomization to investigate the causal link between gut microbiota and diabetic nephropathy. Certain gut bacteria, like Verrucomicrobiae, increase diabetic nephropathy risk, while others may offer protection.
Area of Science:
- Microbiology
- Genetics
- Nephrology
Background:
- Emerging evidence suggests a link between gut microbiota (GM) and diabetic nephropathy (DN) through the
- gut-kidney
- axis.
- However, the causal relationship remains unclear.
Purpose of the Study:
- To investigate the causal relationship between gut microbiota and diabetic nephropathy (DN), including type 1 (T1DN) and type 2 (T2DN) forms.
- To explore the causal links between GM and type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM).
Main Methods:
- A two-sample Mendelian randomization (MR) analysis was performed.
- Utilized summary data from MiBioGen for 211 GM taxa and FinnGen for DN, T1DN, T2DN, T1DM, and T2DM.
- Employed generalized MR analysis and comprehensive sensitivity analyses to ensure result reliability.
Main Results:
- Specific gut bacteria, including Class Verrucomicrobiae, Order Verrucomicrobiales, and Family Verrucomicrobiaceae, were significantly associated with an increased risk of DN.
- Significant associations were found between GM and T2DN, with Class Verrucomimicrobiae, Order Verrucomimicrobiae, Rhodospirillales, and Family Verrucomicroniaceae showing increased risk.
- Eubacteriumprotogenes was associated with a protective effect against T1DN.
Conclusions:
- Identified specific gut microbiota causally linked to DN in both T1DM and T2DM patients.
- Revealed distinct microbial changes in T1DN compared to T2DN, providing insights into subtype-specific GM signatures.
- Confirmed no significant heterogeneity or pleiotropy, supporting the robustness of the findings.
