Mendelian randomization study of inflammatory bowel disease and type 1 diabetes.

IF 3.7 3区医学 Q2 Medicine Endocrine Pub Date : 2024-12-01 Epub Date: 2024-07-31 DOI:10.1007/s12020-024-03919-9

Jing-Yi Zhu, Xinyi Ma, Mu-Yun Liu, Li-Zhe Ma, Xiao-Ru Sun, Mao-Yun Yan, Chunyu Xue, Chang Sun

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Abstract

Purpose: Our purpose was to investigate and test the causal relationship between type 1 diabetes (T1D) and inflammatory bowel disease (IBD) and its major phenotypes, including ulcerative colitis (UC) and Crohn's disease (CD), in two large datasets.

Methods: We obtained IBD samples from the largest publicly available genome-wide association study (GWAS), as well as the FinnGen database and the publicly accessible IEU GWAS database of T1D. We employed a two-sample Mendelian randomization approach to assess bidirectional causality using the inverse variance weighting (IVW) method as the primary outcome.

Results: Genetic predisposition to T1D was associated with reduced risk of IBD (IVW: odds ratio (OR), 0.867; 95% confidence interval (CI), [0.852, 0.883]; P < 0.001), UC (OR = 0.879 [0.823, 0.939], P < 0.001), and CD (OR = 0.925 [0.872, 0.981], P = 0.009). The republication results found IBD genetically possessed negative association with T1D (OR = 0.781 [0.684, 0.891], P < 0.001). Additionally, a meta-analysis of results was conducted to prove the strong evidence between T1D and CD (OR = 0.95 [0.91, 0.98]; p = 0.01).

Conclusions: This study first demonstrated a causal effect of TID on the reduced risk of CD in the mendelian randomization study.

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炎症性肠病与 1 型糖尿病的孟德尔随机研究。

目的：我们的目的是在两个大型数据集中调查和检验1型糖尿病（T1D）与炎症性肠病（IBD）及其主要表型（包括溃疡性结肠炎（UC）和克罗恩病（CD））之间的因果关系：我们从最大的公开全基因组关联研究（GWAS）、FinnGen 数据库和可公开访问的 IEU T1D GWAS 数据库中获得了 IBD 样本。我们采用双样本孟德尔随机化方法，以反向方差加权（IVW）法评估双向因果关系作为主要结果：结果：T1D 的遗传易感性与 IBD 风险的降低相关（IVW：比值比 (OR)，0.867；95% 置信区间 (CI)，[0.852, 0.883]；P）：该研究首次在 "泯灭随机研究 "中证明了 TID 对降低 CD 风险的因果效应。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Endocrine 医学-内分泌学与代谢

CiteScore

6.40

自引率

5.40%

发文量

期刊介绍： Well-established as a major journal in today’s rapidly advancing experimental and clinical research areas, Endocrine publishes original articles devoted to basic (including molecular, cellular and physiological studies), translational and clinical research in all the different fields of endocrinology and metabolism. Articles will be accepted based on peer-reviews, priority, and editorial decision. Invited reviews, mini-reviews and viewpoints on relevant pathophysiological and clinical topics, as well as Editorials on articles appearing in the Journal, are published. Unsolicited Editorials will be evaluated by the editorial team. Outcomes of scientific meetings, as well as guidelines and position statements, may be submitted. The Journal also considers special feature articles in the field of endocrine genetics and epigenetics, as well as articles devoted to novel methods and techniques in endocrinology. Endocrine covers controversial, clinical endocrine issues. Meta-analyses on endocrine and metabolic topics are also accepted. Descriptions of single clinical cases and/or small patients studies are not published unless of exceptional interest. However, reports of novel imaging studies and endocrine side effects in single patients may be considered. Research letters and letters to the editor related or unrelated to recently published articles can be submitted. Endocrine covers leading topics in endocrinology such as neuroendocrinology, pituitary and hypothalamic peptides, thyroid physiological and clinical aspects, bone and mineral metabolism and osteoporosis, obesity, lipid and energy metabolism and food intake control, insulin, Type 1 and Type 2 diabetes, hormones of male and female reproduction, adrenal diseases pediatric and geriatric endocrinology, endocrine hypertension and endocrine oncology.