Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males: potential mechanism of resistance to weight loss among Japanese obese smokersReport as inadecuate




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Tobacco Induced Diseases

, 10:3

First Online: 28 February 2012Received: 25 December 2011Accepted: 28 February 2012DOI: 10.1186-1617-9625-10-3

Cite this article as: Nagayasu, S., Suzuki, S., Yamashita, A. et al. Tob. Induced Dis. 2012 10: 3. doi:10.1186-1617-9625-10-3

Abstract

BackgroundThe 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.

MethodsWe 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.

ResultsIn subjects with BMI below 25 kg-m, 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, 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.

ConclusionsAdipose 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.

KeywordsLeptin Smoking Low-grade inflammation Nicotine ICAM-1 Electronic supplementary materialThe online version of this article doi:10.1186-1617-9625-10-3 contains supplementary material, which is available to authorized users.

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Author: Shintaro Nagayasu - Shigeki Suzuki - Akiko Yamashita - Ataru Taniguchi - Mitsuo Fukushima - Yoshikatsu Nakai - Kazuko Nin -

Source: https://link.springer.com/







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