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Dietary Magnesium Intake and Leukocyte Telomere Attrition in Adults: The Regulatory Role of Serum Tumor Necrosis Factor α.
Mediators of Inflammation ( IF 4.6 ) Pub Date : 2020-05-22 , DOI: 10.1155/2020/7610436
Jie Yu 1 , Haibin Liu 2 , Shuli He 3 , Pingping Li 4 , Chunxiao Ma 5 , Minglei Ma 1 , Yiwen Liu 1 , Lu Lv 1 , Fan Ping 1 , Huabing Zhang 1 , Wei Li 1 , Qi Sun 1 , Lingling Xu 1 , Yuxiu Li 1
Affiliation  

Objectives. In this study, we assessed the effects of dietary magnesium on leukocyte telomere length (LTL). Designs. The current cross-sectional analysis was based on data collected within a type 2 diabetes project. Settings. Dietary magnesium intake is associated with peripheral blood leukocyte telomere length (LTL). However, few epidemiological studies have evaluated the effects of magnesium on LTL in the clinical setting. Participants. This cross-sectional analysis included 467 participants (34.8% men). Measurements. Serum blood lipid profile, HbA1c, oxidative stress, and proinflammatory mediator levels were measured. Detailed dietary data were obtained using a 24 h food recall. LTL was assessed using a real-time PCR assay. Regression models and simple regulatory models were used for data analysis. Results. There was an inverse relationship between dietary magnesium and LTL (), with a between-extreme-quarter difference of -0.55. Conversely, there was a positive relationship between dietary magnesium and serum tumor necrosis factor (TNF) α, with an interquarter difference of 3.79 pmol/mL (). Multivariate regression analysis revealed that the odds ratios (ORs) for shorter LTL and higher serum TNFα increased with magnesium intake, and the ORs of the differences between extreme quartiles were 2.60 (95% confidence interval (CI): 1.31–5.36; ) and 1.98 (95% CI: 1.09–3.59; ). There was a direct negative effect of dietary magnesium intake on LTL (; ), which appeared to be indirectly influenced by TNFα (-0.002 to -0.0005). Conclusions. Dietary magnesium intake may be a critical component of the cellular aging process, and its effect could be partly mediated by TNFα.

中文翻译:

成人膳食镁摄入量和白细胞端粒磨损:血清肿瘤坏死因子 α 的调节作用。

目标。在这项研究中,我们评估了膳食镁对白细胞端粒长度 (LTL) 的影响。设计。当前的横断面分析基于在 2 型糖尿病项目中收集的数据。设置。膳食镁摄入量与外周血白细胞端粒长度 (LTL) 相关。然而,很少有流行病学研究评估了镁在临床环境中对 LTL 的影响。参与者。这项横断面分析包括 467 名参与者(34.8% 男性)。测量. 测量了血清血脂谱、HbA1c、氧化应激和促炎介质水平。使用 24 小时食物召回获得详细的饮食数据。使用实时 PCR 分析评估 LTL。回归模型和简单的监管模型用于数据分析。结果。膳食镁与 LTL 之间存在负相关关系(),极值之间的季度差异为 -0.55。相反,膳食镁与血清肿瘤坏死因子(TNF) α呈正相关,季度间差异为 3.79 pmol/mL()。多元回归分析显示,较短 LTL 和较高血清 TNF α的优势比(ORs)随着镁摄入量的增加而增加,极端四分位数之间差异的 ORs 为 2.60(95% 置信区间(CI):1.31-5.36;)和 1.98 (95% CI: 1.09–3.59;)。膳食镁摄入量对 LTL 有直接的负面影响(; ),这似乎受到 TNF α的间接影响(-0.002 至 -0.0005)。结论。膳食镁摄入量可能是细胞衰老过程的关键组成部分,其作用可能部分由 TNF α介导。
更新日期:2020-05-22
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