Smoking and diabetes: is the association mediated by adiponectin, leptin, or C-reactive protein?
Smoking and diabetes: is the association mediated by adiponectin, leptin, or C-reactive protein?
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吸烟和糖尿病：该关联是由脂联素，瘦素还是C反应蛋白介导的？
DOI：
10.2188/jea.je20140055
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发表时间：
2015
影响因子：
4.7
通讯作者：
Aoyama A
中科院分区：
文献类型：
--
作者：
Hilawe EH;Yatsuya H;Li Y;Uemura M;Wang C;Chiang C;Toyoshima H;Tamakoshi K;Zhang Y;Kawazoe N;Aoyama A
虽然吸烟与2型糖尿病之间的关系已经确立，但其机制尚不清楚。本研究探讨了脂联素、瘦素和c反应蛋白（CRP）浓度在吸烟-糖尿病关联中的可能中介作用。2002年至2011年间，我们随访了3338名年龄在35-66岁之间的日本工人，他们参加了第二次爱知县工人队列研究。我们使用多变量校正Cox回归模型来确定吸烟状况与糖尿病风险之间的风险比和各自的95%置信区间（ci）。采用自举的多重中介模型，通过三种生物标志物估计吸烟对糖尿病间接影响的大小和各自的偏差校正（BC） 95% CIs。与从不吸烟者相比，当前吸烟者（风险比1.75,95% CI 1.25-2.46）和戒烟者（风险比1.54,95% CI 1.07-2.22）患糖尿病的风险显著升高。吸烟通过脂联素水平对糖尿病的间接影响在轻度吸烟者（估计为0.033，BC 95% CI为0.005-0.082）、中度吸烟者（估计为0.044，BC 95% CI为0.010-0.094）和重度吸烟者（估计为0.054，BC 95% CI为0.013-0.113）中具有统计学意义。相比之下，吸烟通过瘦素和CRP水平对糖尿病的间接影响都不显著，因为相应的BC 95% ci为零。在我们的分析中，脂联素浓度似乎部分调节了吸烟对糖尿病的影响，而瘦素和CRP水平则没有。
Although the association between cigarette smoking and risk of type 2 diabetes is well established, its mechanisms are yet to be clarified. This study examined the possible mediating effects of adiponectin, leptin, and C-reactive protein (CRP) concentrations on the smoking-diabetes association. Between 2002 and 2011, we followed 3338 Japanese workers, aged 35–66 years, who were enrolled in the second Aichi workers’ cohort study. We used multivariable-adjusted Cox regression models to determine the hazard ratios and respective 95% confidence intervals (CIs) of the association between smoking status and risk of diabetes. A multiple mediation model with bootstrapping was used to estimate the magnitude and the respective bias-corrected (BC) 95% CIs of the indirect effects of smoking on diabetes through the three biomarkers. Relative to never smokers, the risk of diabetes was significantly elevated in current (hazard ratio 1.75, 95% CI 1.25–2.46) and ex-smokers (hazard ratio 1.54, 95% CI 1.07–2.22). The indirect effects of smoking on diabetes through adiponectin levels were statistically significant among light (point estimate 0.033, BC 95% CI 0.005–0.082), moderate (point estimate 0.044, BC 95% CI 0.010–0.094), and heavy smokers (point estimate 0.054, BC 95% CI 0.013–0.113). In contrast, neither the indirect effects of smoking on diabetes through leptin nor CRP levels were significant, as the corresponding BC 95% CIs included zero. In our analysis, adiponectin concentration appeared to partially mediate the effect of smoking on diabetes, while leptin and CRP levels did not.