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炎症细胞因子在肥胖与疾病关系中的作用及其作用机制。

The Role of Inflammatory Cytokines as Intermediates in the Pathway from Increased Adiposity to Disease.

机构信息

Computational Medicine, Center for Life Course Health Research, Faculty of Medicine, University of Oulu, Oulu, Finland.

Biocenter Oulu, University of Oulu, Oulu, Finland.

出版信息

Obesity (Silver Spring). 2021 Feb;29(2):428-437. doi: 10.1002/oby.23060.

DOI:10.1002/oby.23060
PMID:33491305
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8614117/
Abstract

OBJECTIVE

This study aimed to investigate the role of cytokines as intermediates in the pathway from increased adiposity to disease.

METHODS

BMI and circulating levels of up to 41 cytokines were measured in individuals from three Finnish cohort studies (n = 8,293). Mendelian randomization (MR) was used to assess the impact of BMI on circulating cytokines and the impact of BMI-driven cytokines on risk of obesity-related diseases.

RESULTS

Observationally, BMI was associated with 19 cytokines. For every SD increase in BMI, causal effect estimates were strongest for hepatocyte growth factor, monocyte chemotactic protein-1 (MCP-1), and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and were as ratios of geometric means 1.13 (95% CI: 1.08-1.19), 1.08 (95% CI: 1.04-1.14), and 1.13 (95% CI: 1.04-1.21), respectively. TRAIL was associated with a small increase in the odds of coronary artery disease (odds ratio: 1.03; 95% CI: 1.00-1.06). There was inconsistent evidence for a protective role of MCP-1 against inflammatory bowel diseases.

CONCLUSIONS

Observational and MR estimates of the effect of BMI on cytokine levels were generally concordant. There was little evidence for an effect of raised levels of BMI-driven cytokines on disease. These findings illustrate the challenges of MR when applied in the context of molecular mediation.

摘要

目的

本研究旨在探讨细胞因子作为肥胖程度增加到疾病发生这一途径中间产物的作用。

方法

在来自三个芬兰队列研究的个体中（n=8293），测量了 BMI 和多达 41 种细胞因子的循环水平。孟德尔随机化（MR）用于评估 BMI 对循环细胞因子的影响，以及 BMI 驱动的细胞因子对肥胖相关疾病风险的影响。

结果

观察性研究发现，BMI 与 19 种细胞因子相关。BMI 每增加一个标准差，细胞因子的因果效应估计值最强的是肝细胞生长因子、单核细胞趋化蛋白-1（MCP-1）和肿瘤坏死因子相关凋亡诱导配体（TRAIL），分别为几何均数的 1.13（95%CI：1.08-1.19）、1.08（95%CI：1.04-1.14）和 1.13（95%CI：1.04-1.21）。TRAIL 与冠心病的患病风险略有增加相关（比值比：1.03；95%CI：1.00-1.06）。MCP-1 对炎症性肠病具有保护作用的证据不一致。

结论

BMI 对细胞因子水平的观察性和 MR 估计值通常是一致的。升高的 BMI 驱动细胞因子水平对疾病的影响几乎没有证据。这些发现说明了在分子介导的背景下应用 MR 所面临的挑战。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/b27373c7cfb1/OBY-29-428-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/2d407084cd57/OBY-29-428-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/19289c7de4a8/OBY-29-428-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/4e09ffec6672/OBY-29-428-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/b27373c7cfb1/OBY-29-428-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/2d407084cd57/OBY-29-428-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/19289c7de4a8/OBY-29-428-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/4e09ffec6672/OBY-29-428-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24aa/8614117/b27373c7cfb1/OBY-29-428-g001.jpg

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