Influence of cigarette smoking and inflammatory gene polymorphisms on glycated hemoglobin in the Japanese general population

for the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study Group

Research output: Contribution to journalArticle

Abstract

Objective: Inflammation is closely involved in the development of type 2 diabetes, and cigarette smoking acts as potent inducer of inflammation. We therefore investigated interactions between inflammation-related gene polymorphisms and cigarette smoking on glycated hemoglobin (HbA1c) in the Japanese general population. Method: We conducted a cross-sectional study using data collected from 2619 Japanese (1274 males and 1345 females) 40-69 years of age who participated in baseline survey of the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study (2005-2008). Eight polymorphisms in seven genes (interleukin [IL]-1β, IL-2, IL-4, IL-8, IL-10, IL-13 and tumor necrosis factor-α) were determined using the Invader assay. The interactions of smoking and gene polymorphisms on HbA1c levels were analyzed using multiple linear and logistic regression models and analysis of covariance with adjustment for potential confounders. Results: Among the eight polymorphisms, only one significant interaction was detected for IL-1β T-31C (P < 0.0001). Among the subjects carrying TT genotype, current heavy smokers (≥20 cigarettes/day) had higher HbA1c (5.83 [95% confidence interval 5.67-5.99] %) versus all other smoking status groups (never 5.49 [5.41-5.56] %, former 5.54 [5.43-5.65] %, current moderate [<20 cigarettes/day] 5.50 [5.30-5.69] %), whereas such differences were not observed in the subjects with C allele. The logistic regression analyses regarding high-normal HbA1c levels showed a similar pattern of results. Conclusion: Smoking status did not interact with any other inflammation-related polymorphisms except for IL-1β T-31C. Heavy smokers harboring the TT genotype of IL-1β T-31C polymorphism show a greater adverse effect of smoking on HbA1c levels among Japanese middle-aged subjects.

Original languageEnglish
Pages (from-to)288-295
Number of pages8
JournalPreventive Medicine Reports
Volume3
DOIs
Publication statusPublished - 01-06-2016

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Glycosylated Hemoglobin A
Smoking
Interleukin-1
Population
Genes
Inflammation
Logistic Models
Tobacco Products
Genotype
Regression Analysis
Interleukin-13
Interleukin-8
Interleukin-4
Interleukin-10
Type 2 Diabetes Mellitus
Interleukin-2
Linear Models
Japan
Cohort Studies
Tumor Necrosis Factor-alpha

All Science Journal Classification (ASJC) codes

  • Health Informatics
  • Public Health, Environmental and Occupational Health

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for the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study Group. / Influence of cigarette smoking and inflammatory gene polymorphisms on glycated hemoglobin in the Japanese general population. In: Preventive Medicine Reports. 2016 ; Vol. 3. pp. 288-295.
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title = "Influence of cigarette smoking and inflammatory gene polymorphisms on glycated hemoglobin in the Japanese general population",
abstract = "Objective: Inflammation is closely involved in the development of type 2 diabetes, and cigarette smoking acts as potent inducer of inflammation. We therefore investigated interactions between inflammation-related gene polymorphisms and cigarette smoking on glycated hemoglobin (HbA1c) in the Japanese general population. Method: We conducted a cross-sectional study using data collected from 2619 Japanese (1274 males and 1345 females) 40-69 years of age who participated in baseline survey of the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study (2005-2008). Eight polymorphisms in seven genes (interleukin [IL]-1β, IL-2, IL-4, IL-8, IL-10, IL-13 and tumor necrosis factor-α) were determined using the Invader assay. The interactions of smoking and gene polymorphisms on HbA1c levels were analyzed using multiple linear and logistic regression models and analysis of covariance with adjustment for potential confounders. Results: Among the eight polymorphisms, only one significant interaction was detected for IL-1β T-31C (P < 0.0001). Among the subjects carrying TT genotype, current heavy smokers (≥20 cigarettes/day) had higher HbA1c (5.83 [95{\%} confidence interval 5.67-5.99] {\%}) versus all other smoking status groups (never 5.49 [5.41-5.56] {\%}, former 5.54 [5.43-5.65] {\%}, current moderate [<20 cigarettes/day] 5.50 [5.30-5.69] {\%}), whereas such differences were not observed in the subjects with C allele. The logistic regression analyses regarding high-normal HbA1c levels showed a similar pattern of results. Conclusion: Smoking status did not interact with any other inflammation-related polymorphisms except for IL-1β T-31C. Heavy smokers harboring the TT genotype of IL-1β T-31C polymorphism show a greater adverse effect of smoking on HbA1c levels among Japanese middle-aged subjects.",
author = "{for the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study Group} and Yuichiro Nishida and Megumi Hara and Tatsuhiko Sakamoto and Koichi Shinchi and Sayo Kawai and Mariko Naito and Nobuyuki Hamajima and Aya Kadota and Sadao Suzuki and Rie Ibusuki and Akie Hirata and Miwa Yamaguchi and Nagato Kuriyama and Isao Oze and Haruo Mikami and Michiaki Kubo and Michiaki Kubo",
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Influence of cigarette smoking and inflammatory gene polymorphisms on glycated hemoglobin in the Japanese general population. / for the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study Group.

In: Preventive Medicine Reports, Vol. 3, 01.06.2016, p. 288-295.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Influence of cigarette smoking and inflammatory gene polymorphisms on glycated hemoglobin in the Japanese general population

AU - for the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study Group

AU - Nishida, Yuichiro

AU - Hara, Megumi

AU - Sakamoto, Tatsuhiko

AU - Shinchi, Koichi

AU - Kawai, Sayo

AU - Naito, Mariko

AU - Hamajima, Nobuyuki

AU - Kadota, Aya

AU - Suzuki, Sadao

AU - Ibusuki, Rie

AU - Hirata, Akie

AU - Yamaguchi, Miwa

AU - Kuriyama, Nagato

AU - Oze, Isao

AU - Mikami, Haruo

AU - Kubo, Michiaki

AU - Kubo, Michiaki

PY - 2016/6/1

Y1 - 2016/6/1

N2 - Objective: Inflammation is closely involved in the development of type 2 diabetes, and cigarette smoking acts as potent inducer of inflammation. We therefore investigated interactions between inflammation-related gene polymorphisms and cigarette smoking on glycated hemoglobin (HbA1c) in the Japanese general population. Method: We conducted a cross-sectional study using data collected from 2619 Japanese (1274 males and 1345 females) 40-69 years of age who participated in baseline survey of the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study (2005-2008). Eight polymorphisms in seven genes (interleukin [IL]-1β, IL-2, IL-4, IL-8, IL-10, IL-13 and tumor necrosis factor-α) were determined using the Invader assay. The interactions of smoking and gene polymorphisms on HbA1c levels were analyzed using multiple linear and logistic regression models and analysis of covariance with adjustment for potential confounders. Results: Among the eight polymorphisms, only one significant interaction was detected for IL-1β T-31C (P < 0.0001). Among the subjects carrying TT genotype, current heavy smokers (≥20 cigarettes/day) had higher HbA1c (5.83 [95% confidence interval 5.67-5.99] %) versus all other smoking status groups (never 5.49 [5.41-5.56] %, former 5.54 [5.43-5.65] %, current moderate [<20 cigarettes/day] 5.50 [5.30-5.69] %), whereas such differences were not observed in the subjects with C allele. The logistic regression analyses regarding high-normal HbA1c levels showed a similar pattern of results. Conclusion: Smoking status did not interact with any other inflammation-related polymorphisms except for IL-1β T-31C. Heavy smokers harboring the TT genotype of IL-1β T-31C polymorphism show a greater adverse effect of smoking on HbA1c levels among Japanese middle-aged subjects.

AB - Objective: Inflammation is closely involved in the development of type 2 diabetes, and cigarette smoking acts as potent inducer of inflammation. We therefore investigated interactions between inflammation-related gene polymorphisms and cigarette smoking on glycated hemoglobin (HbA1c) in the Japanese general population. Method: We conducted a cross-sectional study using data collected from 2619 Japanese (1274 males and 1345 females) 40-69 years of age who participated in baseline survey of the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study (2005-2008). Eight polymorphisms in seven genes (interleukin [IL]-1β, IL-2, IL-4, IL-8, IL-10, IL-13 and tumor necrosis factor-α) were determined using the Invader assay. The interactions of smoking and gene polymorphisms on HbA1c levels were analyzed using multiple linear and logistic regression models and analysis of covariance with adjustment for potential confounders. Results: Among the eight polymorphisms, only one significant interaction was detected for IL-1β T-31C (P < 0.0001). Among the subjects carrying TT genotype, current heavy smokers (≥20 cigarettes/day) had higher HbA1c (5.83 [95% confidence interval 5.67-5.99] %) versus all other smoking status groups (never 5.49 [5.41-5.56] %, former 5.54 [5.43-5.65] %, current moderate [<20 cigarettes/day] 5.50 [5.30-5.69] %), whereas such differences were not observed in the subjects with C allele. The logistic regression analyses regarding high-normal HbA1c levels showed a similar pattern of results. Conclusion: Smoking status did not interact with any other inflammation-related polymorphisms except for IL-1β T-31C. Heavy smokers harboring the TT genotype of IL-1β T-31C polymorphism show a greater adverse effect of smoking on HbA1c levels among Japanese middle-aged subjects.

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