TY - JOUR
T1 - Smoking and diabetes
T2 - Is the association mediated by adiponectin, leptin, or C-reactive protein?
AU - Hilawe, Esayas Haregot
AU - Yatsuya, Hiroshi
AU - Li, Yuanying
AU - Uemura, Mayu
AU - Wang, Chaochen
AU - Chiang, Chifa
AU - Toyoshima, Hideaki
AU - Tamakoshi, Koji
AU - Zhang, Yan
AU - Kawazoe, Nobuo
AU - Aoyama, Atsuko
N1 - Publisher Copyright:
© 2014 Esayas Haregot Hilawe et al.
PY - 2015
Y1 - 2015
N2 - Background: 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. Methods: 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 biascorrected (BC) 95% CIs of the indirect effects of smoking on diabetes through the three biomarkers. Results: 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. Conclusions: In our analysis, adiponectin concentration appeared to partially mediate the effect of smoking on diabetes, while leptin and CRP levels did not.
AB - Background: 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. Methods: 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 biascorrected (BC) 95% CIs of the indirect effects of smoking on diabetes through the three biomarkers. Results: 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. Conclusions: In our analysis, adiponectin concentration appeared to partially mediate the effect of smoking on diabetes, while leptin and CRP levels did not.
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U2 - 10.2188/jea.JE20140055
DO - 10.2188/jea.JE20140055
M3 - Article
C2 - 25400076
AN - SCOPUS:84923872990
SN - 0917-5040
VL - 25
SP - 99
EP - 109
JO - Journal of epidemiology
JF - Journal of epidemiology
IS - 2
ER -