Wolf Kathrin, Popp Anita, Schneider Alexandra, Breitner Susanne, Hampel Regina, Rathmann Wolfgang, Herder Christian, Roden Michael, Koenig Wolfgang, Meisinger Christa, Peters Annette
Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Epidemiology II, Neuherberg, Germany
Ludwig-Maximilians-Universität (LMU) Munich, Institute for Medical Informatics, Biometrics and Epidemiology, Munich, Germany.
Diabetes. 2016 Nov;65(11):3314-3326. doi: 10.2337/db15-1567. Epub 2016 Sep 7.
Insulin resistance (IR) is present long before the onset of type 2 diabetes and results not only from inherited and lifestyle factors but also likely from environmental conditions. We investigated the association between modeled long-term exposure to air pollution at residence and biomarkers related to IR, subclinical inflammation, and adipokines. Data were based on 2,944 participants of the KORA (Cooperative Health Research in the Region Augsburg) F4 study conducted in southern Germany (2006-2008). We analyzed associations between individual air pollution concentration estimated by land use regression and HOMA-IR, glucose, insulin, HbA, leptin, and high-sensitivity C-reactive protein levels from fasting samples using multivariable linear regression models. Effect estimates were calculated for the whole study population and subgroups of individuals who did not have diabetes, had prediabetes, or had diabetes. Among all participants, a 7.9 μg/m increment in particulate matter of <10 μm was associated with higher HOMA-IR (15.6% [95% CI 4.0; 28.6]) and insulin (14.5% [3.6; 26.5]). Nitrogen dioxide was associated with HOMA-IR, glucose, insulin, and leptin. Effect estimates for individuals with prediabetes were much larger and highly statistically significant, whereas individuals who did not have diabetes or had diabetes showed rather weak associations. No association was seen for HbA level. Our results suggested an association between long-term exposure to air pollution and IR in the general population that was attributable mainly to individuals with prediabetes.
胰岛素抵抗(IR)在2型糖尿病发病前很久就已存在,其产生不仅源于遗传和生活方式因素,还可能与环境状况有关。我们调查了居住地长期空气污染模型暴露与IR、亚临床炎症和脂肪因子相关生物标志物之间的关联。数据基于在德国南部进行的KORA(奥格斯堡地区合作健康研究)F4研究的2944名参与者(2006 - 2008年)。我们使用多变量线性回归模型分析了通过土地利用回归估算的个体空气污染浓度与空腹样本中HOMA-IR、血糖、胰岛素、糖化血红蛋白(HbA)、瘦素和高敏C反应蛋白水平之间的关联。计算了整个研究人群以及未患糖尿病、患有糖尿病前期或患有糖尿病的个体亚组的效应估计值。在所有参与者中,<10μm颗粒物每增加7.9μg/m³与更高的HOMA-IR(15.6% [95%CI 4.0;28.6])和胰岛素(14.5% [3.6;26.5])相关。二氧化氮与HOMA-IR、血糖、胰岛素和瘦素相关。糖尿病前期个体的效应估计值要大得多且具有高度统计学意义,而未患糖尿病或患有糖尿病的个体显示出的关联相当微弱。未发现与HbA水平有关联。我们的结果表明,一般人群中长期暴露于空气污染与IR之间存在关联,这主要归因于糖尿病前期个体。