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代谢因素不是 2 型糖尿病与骨质疏松症之间关联的直接介导因素。

Metabolic factors are not the direct mediators of the association between type 2 diabetes and osteoporosis.

机构信息

Department of Orthopedics, The First Hospital of Jilin University, Changchun, China.

Department of Gynecology and Obstetrics, Jinan Maternity and Child Care Hospital Affiliated to Shandong First Medical University, Jinan, China.

出版信息

Front Endocrinol (Lausanne). 2024 Jul 25;15:1404747. doi: 10.3389/fendo.2024.1404747. eCollection 2024.

DOI:10.3389/fendo.2024.1404747
PMID:39119008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11306037/
Abstract

OBJECTIVE

The causal relationship between type 2 diabetes mellitus (T2DM) and osteoporosis (OS) remains unclear. This study aims to investigate the causal relationship and explore the potential metabolic mechanism and its mediating role.

METHODS

We conducted a comprehensive study, gathering data on 490,089 T2DM patients from the genome-wide association study (GWAS) database and selecting OS data from FinnGen and MRC-IEU sources, including 212,778 and 463,010 patients, respectively, for causal analysis. Simultaneously, we explored the potential roles of three obesity traits and 30 metabolic and inflammation-related mediating variables in the causal relationship.

RESULTS

There is a strong causal relationship between T2DM and OS. The data from our two different database sources appeared in the same direction, but after correcting for body mass index (BMI), waist circumference (WC), and waist-to-hip ratio (WHR), the direction became the same. T2DM may increase the risk of OS [odds ratio () > 1.5, < 0.001]. Steiger's test results show that there is no reverse causality. No risk factors related to glycolipid metabolism, amino acid metabolism, and inflammation were found to mediate the causal relationship.

CONCLUSION

This study's findings indicate a robust causal relationship between T2DM and OS, influenced by relevant factors such as BMI. Our results shed light on the pathogenesis of OS and underscore the importance for clinicians to treat metabolic disorders to prevent osteoporosis.

摘要

目的

2 型糖尿病（T2DM）与骨质疏松症（OS）之间的因果关系仍不清楚。本研究旨在探讨两者之间的因果关系，并探索潜在的代谢机制及其介导作用。

方法

我们进行了一项全面的研究，从全基因组关联研究（GWAS）数据库中收集了 490089 例 T2DM 患者的数据，并从 FinnGen 和 MRC-IEU 来源中选择了 OS 数据，分别纳入了 212778 例和 463010 例患者进行因果分析。同时，我们探讨了三种肥胖特征和 30 种代谢和炎症相关的中介变量在因果关系中的潜在作用。

结果

T2DM 与 OS 之间存在很强的因果关系。我们从两个不同数据库来源的数据方向一致，但在对体重指数（BMI）、腰围（WC）和腰臀比（WHR）进行校正后，方向变为一致。T2DM 可能会增加发生 OS 的风险[优势比（OR）>1.5，<0.001]。Steiger 检验结果表明不存在反向因果关系。未发现与糖脂代谢、氨基酸代谢和炎症相关的风险因素介导这种因果关系。

结论

本研究结果表明 T2DM 和 OS 之间存在强有力的因果关系，这种关系受到 BMI 等相关因素的影响。我们的研究结果揭示了 OS 的发病机制，并强调了临床医生治疗代谢紊乱以预防骨质疏松症的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/90df21bec6fd/fendo-15-1404747-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/851e3fc67855/fendo-15-1404747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/1770659edd33/fendo-15-1404747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/abc881623ef1/fendo-15-1404747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/663ed8b1ea19/fendo-15-1404747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/636e9e31a288/fendo-15-1404747-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/90df21bec6fd/fendo-15-1404747-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/851e3fc67855/fendo-15-1404747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/1770659edd33/fendo-15-1404747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/abc881623ef1/fendo-15-1404747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/663ed8b1ea19/fendo-15-1404747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/636e9e31a288/fendo-15-1404747-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5aa/11306037/90df21bec6fd/fendo-15-1404747-g006.jpg

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