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Pediatric obesity-related asthma: A prototype of pediatric severe non-T2 asthma.儿童肥胖相关性哮喘:儿童严重非 T2 哮喘的雏形。
Pediatr Pulmonol. 2020 Mar;55(3):809-817. doi: 10.1002/ppul.24600. Epub 2020 Jan 8.
3
Association of Metformin Initiation and Risk of Asthma Exacerbation. A Claims-based Cohort Study.二甲双胍起始治疗与哮喘恶化风险的相关性:基于索赔数据的队列研究。
Ann Am Thorac Soc. 2019 Dec;16(12):1527-1533. doi: 10.1513/AnnalsATS.201812-897OC.
4
Nonfasting versus fasting lipid profile for cardiovascular risk prediction.非空腹与空腹血脂谱用于心血管风险预测。
Pathology. 2019 Feb;51(2):131-141. doi: 10.1016/j.pathol.2018.09.062. Epub 2018 Dec 3.
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Nonfasting lipid testing: the new standard for cardiovascular risk assessment.非空腹血脂检测:心血管风险评估的新标准。
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7
Non-atopic rhinitis at age 6 is associated with subsequent development of asthma.6 岁时的非过敏性鼻炎与随后哮喘的发展有关。
Clin Exp Allergy. 2019 Jan;49(1):35-43. doi: 10.1111/cea.13276. Epub 2018 Oct 9.
8
Lung function trajectories from pre-school age to adulthood and their associations with early life factors: a retrospective analysis of three population-based birth cohort studies.从学前到成年的肺功能轨迹及其与早期生活因素的关联:三项基于人群的出生队列研究的回顾性分析。
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Obesity and asthma.肥胖与哮喘。
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Genetic Evidence That Carbohydrate-Stimulated Insulin Secretion Leads to Obesity.遗传证据表明,碳水化合物刺激胰岛素分泌会导致肥胖。
Clin Chem. 2018 Jan;64(1):192-200. doi: 10.1373/clinchem.2017.280727.

儿童早期高胰岛素水平与后续哮喘风险有关,与体重指数无关。

High Insulin in Early Childhood Is Associated with Subsequent Asthma Risk Independent of Body Mass Index.

机构信息

Asthma and Airway Disease Research Center, University of Arizona, Tucson, Ariz.

University of Bristol, Avon, United Kingdom.

出版信息

J Allergy Clin Immunol Pract. 2022 Mar;10(3):785-792.e5. doi: 10.1016/j.jaip.2021.09.047. Epub 2021 Oct 14.

DOI:10.1016/j.jaip.2021.09.047
PMID:34656798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9059620/
Abstract

BACKGROUND

Asthma and obesity are major, interconnected public health challenges that usually have their origins in childhood, and for which the relationship is strengthened among those with insulin resistance.

OBJECTIVE

To determine whether high insulin in early life confers increased longitudinal risk for asthma independent of body mass index.

METHODS

The study used data from the Tucson Children's Respiratory Study (TCRS) and the Avon Longitudinal Study of Parents and Children (ALSPAC). Nonfasting insulin was measured in TCRS participants at age 6 years and fasting insulin in ALSPAC participants at age 8 years. Physician-diagnosed active asthma was determined at baseline and at subsequent assessments up to age 36 years in TCRS and 17 years in ALSPAC.

RESULTS

In TCRS, high insulin (upper quartile) at age 6 years was associated with increased odds of having active asthma from ages 8 to 36 years compared with low insulin (odds ratio,1.98; 95% CI, 1.28-3.05; P = .002). Similarly, in ALSPAC, high insulin was associated with a significantly higher risk of active asthma from ages 11 to 17 years compared with low insulin (odds ratio, 1.59; 95% CI, 1.12-2.27; P = .009). These findings were independent of baseline body mass index in both cohorts, and were not related to other demographic and asthma risk factors nor other tested markers of systemic inflammation and metabolic syndrome.

CONCLUSIONS

In 2 separate birth cohorts, higher blood insulin level in early childhood was associated with increased risk of active asthma through adolescence and adulthood, independent of body mass index. High insulin indicates a novel mechanism for asthma development, which may be a target for intervention.

摘要

背景

哮喘和肥胖是两个主要的、相互关联的公共卫生挑战,它们通常起源于儿童期,而在胰岛素抵抗患者中,两者的关系更为密切。

目的

确定生命早期的高胰岛素是否会独立于体重指数增加哮喘的纵向风险。

方法

该研究使用了图森儿童呼吸研究(TCRS)和雅芳纵向研究父母和孩子(ALSPAC)的数据。在 TCRS 参与者中,在 6 岁时测量非禁食胰岛素,在 ALSPAC 参与者中,在 8 岁时测量禁食胰岛素。在 TCRS 中,在基线和随后的评估中确定了医生诊断的活动性哮喘,直到 36 岁,而在 ALSPAC 中则为 17 岁。

结果

在 TCRS 中,与低胰岛素相比,6 岁时的高胰岛素(上四分位数)与 8 至 36 岁时发生活动性哮喘的几率增加有关(比值比,1.98;95%置信区间,1.28-3.05;P=0.002)。同样,在 ALSPAC 中,与低胰岛素相比,高胰岛素与 11 至 17 岁时发生活动性哮喘的风险显著增加相关(比值比,1.59;95%置信区间,1.12-2.27;P=0.009)。这两个队列中的发现都独立于基线体重指数,并且与其他人口统计学和哮喘危险因素以及其他测试的系统性炎症和代谢综合征标志物无关。

结论

在两个独立的出生队列中,生命早期的血液胰岛素水平较高与青少年和成年期活动性哮喘的风险增加相关,与体重指数无关。高胰岛素提示哮喘发病的新机制,可能是干预的目标。