TY - JOUR
T1 - Nicotine may affect the secretion of adipokines leptin, resistin, and visfatin through activation of KATP channel
AU - Bai, Xiao Jun
AU - Fan, Li Hong
AU - He, Ying
AU - Ren, Jie
AU - Xu, Wei
AU - Liang, Qi
AU - Li, Hong Bing
AU - Huo, Jian Hua
AU - Bai, Ling
AU - Tian, Hong Yan
AU - Fan, Fen Ling
AU - Ma, Ai Qun
N1 - Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2016/6/1
Y1 - 2016/6/1
N2 - Objective: It 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. Methods: The 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. Results: Compared 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). Conclusions: Nicotine may affect the secretion of adipokines leptin, resistin, and visfatin through activation of KATP channel.
AB - Objective: It 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. Methods: The 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. Results: Compared 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). Conclusions: Nicotine may affect the secretion of adipokines leptin, resistin, and visfatin through activation of KATP channel.
KW - Adipocytes
KW - Adipokines
KW - KATP channel
KW - Smoking
UR - https://www.scopus.com/pages/publications/84961801296
U2 - 10.1016/j.nut.2015.12.001
DO - 10.1016/j.nut.2015.12.001
M3 - 文章
C2 - 26837599
AN - SCOPUS:84961801296
SN - 0899-9007
VL - 32
SP - 645
EP - 648
JO - Nutrition
JF - Nutrition
IS - 6
ER -
