Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China.
Department of Biostatistics, School of Public Health, Shandong University, Jinan, China.
Diabetes Obes Metab. 2018 Jul;20(7):1578-1584. doi: 10.1111/dom.13259. Epub 2018 Mar 11.
Despite the inverse association between cigarette smoking and body mass index (BMI), it is unknown whether the effect of smoking on insulin is mediated through decreased BMI. This study aims to examine the temporal relationship between BMI and insulin, the impact of smoking on this relationship and the mediation effect of BMI on the association between smoking and insulin levels.
The longitudinal cohort consisted of 1121 adults (807 white and 314 black participants, mean age, 42.0 years at follow-up) for whom BMI and fasting insulin were measured twice, with an average follow-up period of 17.1 years. Cross-lagged panel and mediation analysis models were used to examine the temporal relationship between BMI and insulin, and the mediation effect of BMI on the smoking-insulin association.
Smoking was inversely associated with insulin (regression coefficient, -0.073; P = .015 at baseline and -0.121; P < .001 at follow-up), adjusting for age, race and gender. After additional adjustment for follow-up periods, the cross-lagged path coefficient from BMI to insulin (β, 0.226; P < .001) was significantly greater than that from insulin to BMI (β, -0.029; P = .208), with P < .001 for the difference. The path coefficient from BMI to insulin was significantly greater in non-smokers (β, 0.273; P < .001) than in smokers (β, 0.122; P = .046), with P = .013 for the difference. The mediation effect of BMI on the smoking-insulin association was estimated at 53.4% (P = .030) at baseline and 58.7% (P < .001) at follow-up.
These findings suggest that cigarette smoking has a significant impact on the one-directional relationship from BMI to insulin. The insulin-lowering effect of smoking is predominantly mediated through decreased BMI as the result of smoking.
尽管吸烟与体重指数（BMI）呈反比关系，但尚不清楚吸烟对胰岛素的影响是否通过 BMI 的降低来介导。本研究旨在检验 BMI 和胰岛素之间的时间关系，吸烟对这种关系的影响，以及 BMI 对吸烟与胰岛素水平之间关联的中介作用。
该纵向队列包括 1121 名成年人（807 名白人和 314 名黑人参与者，随访时平均年龄为 42.0 岁），他们的 BMI 和空腹胰岛素被测量了两次，平均随访时间为 17.1 年。交叉滞后面板和中介分析模型用于检验 BMI 和胰岛素之间的时间关系，以及 BMI 对吸烟与胰岛素关联的中介作用。
吸烟与胰岛素呈负相关（回归系数，-0.073；P =.015 时为基线，-0.121；P <.001 时为随访），调整了年龄、种族和性别。在进一步调整随访期后，从 BMI 到胰岛素的交叉滞后路径系数（β，0.226；P <.001）显著大于从胰岛素到 BMI 的路径系数（β，-0.029；P =.208），差异具有统计学意义（P <.001）。在非吸烟者中，从 BMI 到胰岛素的路径系数显著大于吸烟者（β，0.273；P <.001），差异具有统计学意义（P =.013）。BMI 对吸烟与胰岛素关联的中介作用在基线时估计为 53.4%（P =.030），在随访时估计为 58.7%（P <.001）。
这些发现表明，吸烟对 BMI 到胰岛素的单向关系有显著影响。吸烟的降胰岛素作用主要通过 BMI 的降低来介导，这是吸烟的结果。
