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Clinical and Experimental Hepatology
eISSN: 2449-8238
ISSN: 2392-1099
Clinical and Experimental Hepatology
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Sarajevo Declaration on Integrity and Visibility of Scholarly Publications
1/2025
vol. 11
 
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abstract:
Original paper

Identifying the genetic link between type 1 diabetes and autoimmune liver diseases

Guo Yu
1
,
Tao Dong
1
,
Haoyuan Gu
1
,
Depeng Liang
2
,
Liming Song
3
,
Jijing Shi
4
,
Xibin Duan
3
,
Chao Ma
4

  1. Xinxiang Medical College, China
  2. Zhengzhou University, China
  3. Zhengzhou Central Hospital Affiliated to Zhengzhou University, China
  4. The First People’s Hospital of Zhengzhou, China
Clin Exp HEPATOL 2025; 11, 1: 52-60
DOI: https://doi.org/10.5114/ceh.2025.149078
Online publish date: 2025/03/31
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Introduction:
It appears that type 1 diabetes mellitus (T1DM) and autoimmune liver diseases (AILDs) are associated, but there is no evidence linking them causally or in a specific direction. This study aims to evaluate the causal relationship between T1DM and AILDs.

Material and methods:
We performed a two-sample Mendelian randomization (MR) analysis. Following thorough evaluation, the dataset from the genome-wide association study was utilized to identify potential candidate single nucleotide polymorphisms. Inverse variance weighting (IVW) served as the primary analytical method, complemented by four sensitivity analysis approaches to evaluate result robustness.

Results:
Mendelian randomization analysis demonstrated a significant positive causal association between genetically elevated risk of T1DM and autoimmune hepatitis (AIH) (OR = 1.168, 95% CI: 1.060-1.287, p = 0.001), primary biliary cholangitis (PBC) (OR = 1.186, 95% CI: 1.050-1.341, p = 0.006), as well as primary sclerosing cholangitis (PSC) (OR = 1.291, 95% CI: 1.016-1.642, p = 0.037). MR-Egger regression analysis suggested a potential influence of horizontal pleiotropy on the causal association for these conditions (AIH: intercept = –0.026, p = 0.451; PBC: intercept = 0.014, p = 0.745; PSC: intercept = –0.013, p = 0.862). Sensitivity analysis utilizing the leave-one-out method supported the robustness of the Mendelian randomization findings. Conversely, reverse Mendelian randomization analysis revealed that genetically predisposed PBC also raises the likelihood of developing T1DM (OR = 1.236, 95% CI: 1.085-1.407, p = 0.001). Conversely, no causal association was found between AIH and T1DM (OR = 1.032, 95% CI: 0.983-1.084, p = 0.207) or between PSC and T1DM (OR = 0.989, 95% CI: 0.849-1.152, p = 0.888).

Conclusions:
Employing two-sample MR analysis, we explored the association between T1DM and AILDs, finding that T1DM elevates the risk of AIH, PBC, and PSC. Further elucidation of the genomic landscape of T1DM and AILDs necessitates large-scale cross-disease genome-wide association studies (GWAS).

keywords:

type 1 diabetes mellitus, autoimmune liver diseases, Mendelian randomization, causal relationship, genome-wide association study
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