Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males: Potential mechanism of resistance to weight loss among Japanese obese smokers

Shintaro Nagayasu, Shigeki Suzuki, Akiko Yamashita, Ataru Taniguchi, Mitsuo Fukushima, Yoshikatsu Nakai, Kazuko Nin, Naoya Watanabe, Shoichiro Nagasaka, Daisuke Yabe, Fusanori Nishimura

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Background: The effect of smoking on leptin regulation is controversial. Smoking may induce low-grade inflammation. Recent series of studies indicated the critical role of macrophage migration in the establishment of adipose tissue inflammation. In this study, we aimed to see the effects of smoking and inflammation on leptin regulation both at cellular and epidemiological levels. Methods. We compared the concentration of inflammatory markers and serum leptin levels among Japanese male subjects. Additionally, leptin and intercellular adhesion molecule (ICAM) -1 gene expression was assessed in adipocytes co-cultured with or without macrophages in the presence or absence of nicotine and/or lipopolysaccharide (LPS). Results: In subjects with BMI below 25 kg/m 2, both WBC counts and soluble-ICAM-1 levels are significantly higher in smokers than in non-smokers. However, leptin concentration did not differ according to smoking status. However, in subjects with BMI over 25 kg/m 2, smokers exhibited significantly lower serum leptin level as well as higher WBC counts and s-ICAM-1 concentration as compared with non-smokers. Leptin gene expression was markedly suppressed in adipocytes co-cultured with macrophages than in adipocyte culture alone. Furthermore, nicotine further suppressed leptin gene expression. ICAM-1 gene expression was markedly up-regulated in adipocytes co-cultured with macrophages when stimulated with LPS. Conclusions: Adipose tissue inflammation appears to down-regulate leptin expression in adipose tissues. Nicotine further suppresses leptin expression. Thus, both smoking and inflammation may diminish leptin effect in obese subjects. Therefore, obese, but not normal weight, smokers might be more resistant to weight loss than non-smokers.

Original languageEnglish
Article number3
JournalTobacco Induced Diseases
Volume10
Issue number1
DOIs
Publication statusPublished - Feb 29 2012

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Leptin
Adipose Tissue
smoking
Weight Loss
Smoking
Inflammation
nicotine
Intercellular Adhesion Molecule-1
Adipocytes
Macrophages
Nicotine
regulation
Gene Expression
Lipopolysaccharides
migration
Down-Regulation
Biomarkers
Weights and Measures

All Science Journal Classification (ASJC) codes

  • Health(social science)
  • Medicine (miscellaneous)
  • Public Health, Environmental and Occupational Health

Cite this

Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males : Potential mechanism of resistance to weight loss among Japanese obese smokers. / Nagayasu, Shintaro; Suzuki, Shigeki; Yamashita, Akiko; Taniguchi, Ataru; Fukushima, Mitsuo; Nakai, Yoshikatsu; Nin, Kazuko; Watanabe, Naoya; Nagasaka, Shoichiro; Yabe, Daisuke; Nishimura, Fusanori.

In: Tobacco Induced Diseases, Vol. 10, No. 1, 3, 29.02.2012.

Research output: Contribution to journalArticle

Nagayasu, Shintaro ; Suzuki, Shigeki ; Yamashita, Akiko ; Taniguchi, Ataru ; Fukushima, Mitsuo ; Nakai, Yoshikatsu ; Nin, Kazuko ; Watanabe, Naoya ; Nagasaka, Shoichiro ; Yabe, Daisuke ; Nishimura, Fusanori. / Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males : Potential mechanism of resistance to weight loss among Japanese obese smokers. In: Tobacco Induced Diseases. 2012 ; Vol. 10, No. 1.
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AU - Taniguchi, Ataru

AU - Fukushima, Mitsuo

AU - Nakai, Yoshikatsu

AU - Nin, Kazuko

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AU - Yabe, Daisuke

AU - Nishimura, Fusanori

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AB - Background: The effect of smoking on leptin regulation is controversial. Smoking may induce low-grade inflammation. Recent series of studies indicated the critical role of macrophage migration in the establishment of adipose tissue inflammation. In this study, we aimed to see the effects of smoking and inflammation on leptin regulation both at cellular and epidemiological levels. Methods. We compared the concentration of inflammatory markers and serum leptin levels among Japanese male subjects. Additionally, leptin and intercellular adhesion molecule (ICAM) -1 gene expression was assessed in adipocytes co-cultured with or without macrophages in the presence or absence of nicotine and/or lipopolysaccharide (LPS). Results: In subjects with BMI below 25 kg/m 2, both WBC counts and soluble-ICAM-1 levels are significantly higher in smokers than in non-smokers. However, leptin concentration did not differ according to smoking status. However, in subjects with BMI over 25 kg/m 2, smokers exhibited significantly lower serum leptin level as well as higher WBC counts and s-ICAM-1 concentration as compared with non-smokers. Leptin gene expression was markedly suppressed in adipocytes co-cultured with macrophages than in adipocyte culture alone. Furthermore, nicotine further suppressed leptin gene expression. ICAM-1 gene expression was markedly up-regulated in adipocytes co-cultured with macrophages when stimulated with LPS. Conclusions: Adipose tissue inflammation appears to down-regulate leptin expression in adipose tissues. Nicotine further suppresses leptin expression. Thus, both smoking and inflammation may diminish leptin effect in obese subjects. Therefore, obese, but not normal weight, smokers might be more resistant to weight loss than non-smokers.

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