阻塞性睡眠呼吸暂停患者载脂蛋白 E 与胰岛素抵抗之间的关系:一项大规模横断面研究。

IF 3.9 2区 医学 Q2 NUTRITION & DIETETICS
ZhiCheng Wei, Ling Tian, Huajun Xu, Chenyang Li, Kejia Wu, Huaming Zhu, Jian Guan, Yafeng Yu, Di Qian, Xinyi Li
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引用次数: 0

摘要

背景:阻塞性睡眠呼吸暂停(OSA)通常与胰岛素抵抗(IR)和血脂异常有关。载脂蛋白 E(APOE)在脂质代谢中发挥着重要作用。该研究旨在基于大规模的 OSA 患者人群,厘清 IR 与 APOE 之间的多因素关系:方法:最终共纳入 5,591 名因 OSA 诊断而接受多导睡眠图检查的参与者。我们收集了每位参与者的人体测量、空腹生化和多导睡眠图数据。我们进行了线性回归分析,以评估 APOE、IR 和睡眠呼吸相关参数之间的关系。逻辑回归、限制性立方样条曲线(RCS)和中介分析用于探讨 OSA 患者 APOE 与 IR 之间的关系:结果:OSA严重程度的增加与肥胖程度的增加、更明显的血脂异常以及更高水平的APOE和IR有关。APOE与呼吸暂停-低通气指数(AHI)、氧饱和度指数(ODI)和微呼吸指数(MAI)呈正相关,即使在调整了年龄、性别、体重指数、吸烟和饮酒水平之后也是如此(β=0.107,β=0.102,β=0.075,均为P 结论:该研究表明,APOE与呼吸暂停-低通气指数(AHI)、氧饱和度指数(ODI)和微呼吸指数(MAI)呈正相关,即使在调整了年龄、性别、体重指数、吸烟和饮酒水平之后也是如此:本研究表明,APOE是导致IR的危险因素;此外,IR在男性OSA和APOE之间起着中介作用。APOE、IR 和 OSA 呈非线性和多阶段关系。综上所述,这些观察结果揭示了 OSA 患者体内代谢紊乱的复杂关系,这将有助于开发新的治疗方法,并加深对 OSA 全身影响的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Relationships between apolipoprotein E and insulin resistance in patients with obstructive sleep apnoea: a large-scale cross-sectional study.

Background: Obstructive sleep apnoea (OSA) is commonly associated with insulin resistance (IR) and dyslipidaemia. Apolipoprotein E (APOE) plays important roles in lipid metabolism. The study aimed to disentangle the multifactorial relationships between IR and APOE based on a large-scale population with OSA.

Methods: A total of 5,591 participants who underwent polysomnography for OSA diagnosis were finally enrolled. We collected anthropometric, fasting biochemical and polysomnographic data for each participant. Linear regression analysis was performed to evaluate the relationships between APOE, IR, and sleep breathing-related parameters. Logistic regression, restricted cubic spline (RCS) and mediation analyses were used to explore relationships between APOE and IR in patients with OSA.

Results: Increasing OSA severity was associated with greater obesity, more obvious dyslipidaemia, and higher levels of APOE and IR. APOE was positively correlated with the apnoea-hypopnoea index (AHI), oxygen desaturation index (ODI) and microarousal index (MAI) even after adjusting for age, sex, body mass index, and smoking and drinking levels (β = 0.107, β = 0.102, β = 0.075, respectively, all P < 0.001). The risks of IR increased from the first to fourth quartiles of APOE (odds ratio (OR) = 1.695, 95% CI: 1.425-2.017; OR = 2.371, 95% confidence interval (CI): 2.009-2.816; OR = 3.392, 95% CI: 2.853-4.032, all P < 0.001) after adjustments. RCS analysis indicated non-linear and dose response relationships between APOE, AHI, ODI, MAI and insulin resistance. Mediation analyses showed that HOMA-IR explained 9.1% and 10% of the association between AHI, ODI and APOE. The same trends were observed in men, but not in women.

Conclusions: This study showed that APOE is a risk factor for IR; moreover, IR acts as a mediator between OSA and APOE in men. APOE, IR, and OSA showed non-linear and multistage relationships. Taken together, these observations revealed the complex relationships of metabolic disorders in patients with OSA, which could lead to the development of new treatment modalities and a deeper understanding of the systemic impact of OSA.

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来源期刊
Nutrition & Metabolism
Nutrition & Metabolism 医学-营养学
CiteScore
8.40
自引率
0.00%
发文量
78
审稿时长
4-8 weeks
期刊介绍: Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.
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