■观察性研究发现,肥胖与非化脓性中耳炎(NSOM)的发展有关,但因果关系和发病机制尚不清楚。这项研究旨在调查肥胖之间的关系,脂质代谢,和NSOM在遗传水平上。
■我们进行了双向双样本孟德尔随机化(MR)研究,以检查肥胖之间的因果关系,脂质代谢相关因素,和NSOM,使用从IEU开放全基因组关联研究(GWAS)项目获得的数据集。此外,我们对血脂指标进行了多变量MR(MVMR)分析,以验证结果.然后,我们将肥胖或体重指数(BMI)用作暴露量,将NSOM用作结果,以寻找脂质和脂肪因子中可能的介质。
■使用NSOM作为结果,我们发现了9个与肥胖和脂质代谢相关的阳性暴露结果。其中,肥胖,BMI,身体脂肪百分比,腰围,臀围,抵抗素是危险因素,而载脂蛋白A1(apoA1),高密度脂蛋白胆固醇(HDL-C),神经生长因子(NGF)为保护因子。然后,我们使用肥胖和脂质代谢相关因素作为结果,使用NSOM作为暴露量进行MR分析,未能取得积极成果。在MVMR分析中,我们发现,在校正了其他潜在的混杂因素后,HDL胆固醇和apoA1仍然与NSOM有因果关系.同时,当肥胖或BMI被用作暴露和NSOM作为结果时,HDL胆固醇或apoA1通过两步MR分析作为介质。调解的MR分析,肥胖,BMI降低了HDL或apoA1的产生,它们是影响NSOM发展的保护因素。
■在遗传水平上,肥胖和肥胖可能促进NSOM的发展,而NSOM对肥胖和肥胖没有影响。肥胖还可以通过降低HDL胆固醇/apoA1来促进NSOM的进展。抵抗素可能是NSOM的潜在危险因素,而NGF可能是一个潜在的保护因子。
UNASSIGNED: Observational studies have found that obesity is associated with the development of non-suppurative otitis media (NSOM), but the causality and pathogenesis are unclear. This study aimed to investigate the association between obesity, lipid metabolism, and NSOM at the genetic level.
UNASSIGNED: We performed a bidirectional two-sample Mendelian randomization (MR) study to examine the causal relationship between obesity, lipid metabolism-related factors, and NSOM by using the datasets obtained from the IEU Open genome-wide association studies (GWAS) Project. Furthermore, a multivariate MR (MVMR) analysis on lipid indicators was conducted to validate the results. We then used obesity or body mass index (BMI) as the exposure and NSOM as the outcome to search for possible mediators in lipids and adipokines.
UNASSIGNED: Using NSOM as the outcome, we found nine positive exposure results related to obesity and lipid metabolism. Among them, obesity, BMI, body fat percentage, waist circumference, hip circumference, and resistin were risk factors, while apolipoprotein A1 (apoA1), high-density lipoprotein cholesterol (HDL-C), and nerve growth factor (NGF) were protective factors. Then, we used the obesity and lipid metabolism-related factors as outcomes and NSOM as the exposure to perform the MR analysis, which failed to obtain positive results. In the MVMR analysis, we found that HDL cholesterol and apoA1 remained causally associated with NSOM after correction for other potential confounders. Simultaneously, when obesity or BMI was used as the exposure and NSOM as the outcome, HDL cholesterol or apoA1 served as mediators through a two-step MR analysis. The MR analysis for mediation, obesity, and BMI reduced the production of HDL or apoA1, which served as protective factors affecting the development of NSOM.
UNASSIGNED: At the genetic level, obesity and adiposity may promote the development of NSOM, while NSOM has no effect on obesity and adiposity. Obesity can also encourage the progress of NSOM by reducing HDL cholesterol/apoA1. Resistin may be a potential risk factor for NSOM, whereas NGF may be a potential protective factor.