Smoking and diabetes

Is the association mediated by adiponectin, leptin, or C-reactive protein?

Esayas Haregot Hilawe, Hiroshi Yatsuya, Enei Ri, Mayu Uemura, Chaochen Wang, Chifa Chiang, Hideaki Toyoshima, Koji Tamakoshi, Yan Zhang, Nobuo Kawazoe, Atsuko Aoyama

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)99-109
Number of pages11
JournalJournal of epidemiology
Volume25
Issue number2
DOIs
Publication statusPublished - 01-01-2015

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Adiponectin
Leptin
C-Reactive Protein
Smoking
Confidence Intervals
Proportional Hazards Models
Type 2 Diabetes Mellitus
Cohort Studies
Biomarkers
Light

All Science Journal Classification (ASJC) codes

  • Epidemiology

Cite this

Hilawe, Esayas Haregot ; Yatsuya, Hiroshi ; Ri, Enei ; Uemura, Mayu ; Wang, Chaochen ; Chiang, Chifa ; Toyoshima, Hideaki ; Tamakoshi, Koji ; Zhang, Yan ; Kawazoe, Nobuo ; Aoyama, Atsuko. / Smoking and diabetes : Is the association mediated by adiponectin, leptin, or C-reactive protein?. In: Journal of epidemiology. 2015 ; Vol. 25, No. 2. pp. 99-109.
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abstract = "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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Hilawe, EH, Yatsuya, H, Ri, E, Uemura, M, Wang, C, Chiang, C, Toyoshima, H, Tamakoshi, K, Zhang, Y, Kawazoe, N & Aoyama, A 2015, 'Smoking and diabetes: Is the association mediated by adiponectin, leptin, or C-reactive protein?', Journal of epidemiology, vol. 25, no. 2, pp. 99-109. https://doi.org/10.2188/jea.JE20140055

Smoking and diabetes : Is the association mediated by adiponectin, leptin, or C-reactive protein? / Hilawe, Esayas Haregot; Yatsuya, Hiroshi; Ri, Enei; Uemura, Mayu; Wang, Chaochen; Chiang, Chifa; Toyoshima, Hideaki; Tamakoshi, Koji; Zhang, Yan; Kawazoe, Nobuo; Aoyama, Atsuko.

In: Journal of epidemiology, Vol. 25, No. 2, 01.01.2015, p. 99-109.

Research output: Contribution to journalArticle

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 - Ri, Enei

AU - Uemura, Mayu

AU - Wang, Chaochen

AU - Chiang, Chifa

AU - Toyoshima, Hideaki

AU - Tamakoshi, Koji

AU - Zhang, Yan

AU - Kawazoe, Nobuo

AU - Aoyama, Atsuko

PY - 2015/1/1

Y1 - 2015/1/1

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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