• Xiao-Jun Bai, Li-Hong Fan, Ying He, Jie Ren, Wei Xu, Qi Liang, Hong-Bing Li, Jian-Hua Huo, Ling Bai, Hong-Yan Tian, Fen-Ling Fan, and Ai-Qun Ma.
• Department of Cardiology, The First Affiliated Hospital Xi'an Jiao Tong University, Xi'an City, Shaanxi Province, China.
• Nutrition. 2016 Jun 1; 32 (6): 645-8.

ObjectiveIt has been confirmed that adipokines are associated with atherosclerosis. Cigarette smoking was found to possibly influence adipokine secretion. However, the precise role of smoking in adipokine secretion and the underlying mechanisms are largely unknown. The aim of this study was to determine whether nicotine, the principal active ingredient of cigarettes, can influence adipokine secretion and its potential mechanism.MethodsThe present study consecutively enrolled 96 men, including 50 smokers with early atherosclerosis and 46 nonsmokers. Serum adipokines, including leptin, resistin, and visfatin, were determined with enzyme-linked immunosorbent assay in all participants. Furthermore, the effect of nicotine on secretion of these adipokines was examined in differentiated 3T3-L1 preadipocytes under the conditions of ATP-dependent potassium (KATP) channel blocked or unblocked.ResultsCompared with the control group, serum levels of leptin, resistin, and visfatin in smokers were significantly higher. In 3T3-L1 adipocytes, nicotine treatment significantly increased the levels of these adipokines (P = 0.014, 0.001, and 0.029, respectively). When the KATP channel was blocked, secretion of resistin and visfatin was reduced (P < 0.001), but no change was found in the leptin secretion (P = 0.522).ConclusionsNicotine may affect the secretion of adipokines leptin, resistin, and visfatin through activation of KATP channel.Copyright © 2016 Elsevier Inc. All rights reserved.

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