RESEARCH PAPER
Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males: potential mechanism of resistance to weight loss among Japanese obese smokers
| 1 | Department of Dental Science for Health Promotion, Hiroshima University
Graduate School of Biomedical Sciences, 1-2-3 Kasumi, Minami-ku, 734-8553
Hiroshima, Japan |
| 2 | Division of Diabetes and Endocrinology, Kyoto Preventive
Medical Center, 28 Nishinokyo, Samaryocho, Nakagyo-ku, Kyoto 604-8091,
Japan |
| 3 | Division of Clinical Nutrition and Internal Medicine, Okayama
Prefectural University, 111 Kuboki, Soja-city, Okayama 719-1197, Japan |
| 4 | Kyoto Institute of Health Science, Karasumaoike-Higashi, Nakagyo-ku, Kyoto 604-0845, Japan |
| 5 | Human health Sciences, Graduate School of medicine,
Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan |
| 6 | Health Care and Promotion Center, Yodogawa Christian Hospital, 2-9-26
Awaji, Higashiyodogawa-ku, Osaka 533-0032, Japan |
| 7 | Division of
Endocrinology and Metabolism, Department of Medicine, Jichi Medical
University, 3311-1 Yakushiji, Shimotsuke-city 329-0498, Japan |
| 8 | Division of
Diabetes, Clinical Nutrition and Endocrinology, Kansai Electric Power Hospital,
2-1-7 Fukushima, Fukushima-ku, Osaka 553-0003, Japan |
Publish date: 2012-02-28
Tobacco Induced Diseases 2012;10(February):3
KEYWORDS:
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/m2 , 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/m2 , 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 nonsmokers.
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/m2 , 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/m2 , 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 nonsmokers.
CORRESPONDING AUTHOR:
Fusanori Nishimura
Department of Dental Science for Health Promotion, Hiroshima University
Graduate School of Biomedical Sciences, 1-2-3 Kasumi, Minami-ku, 734-8553
Hiroshima, Japan
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Are leptin levels a cause or an indicator of cardiovascular risk? Sait Demirkol, Mustafa Cakar, Sevket Balta, Murat Unlu Revista Portuguesa de Cardiologia |
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