Li Hong Fan1, Ying He2, Wei Xu3, Hong Yan Tian3, Yan Zhou4, Qi Liang3, Xin Huang3, Jian Hua Huo3, Hong Bin Li3, Ling Bai3, Ai Qun Ma3. 1. Department of Cardiology, The First Affiliated Hospital of Medicine College, Xi'an Jiao Tong University, Xi'an City, Shaanxi Province, China. Electronic address: Doctorfan@163.com. 2. Medical College, Xi'an Jiao Tong University, Xi'an City, Shaanxi Province, China. 3. Department of Cardiology, The First Affiliated Hospital of Medicine College, Xi'an Jiao Tong University, Xi'an City, Shaanxi Province, China. 4. Department of Dermatology, The First Affiliated Hospital of Medicine College, Xi'an Jiaotong University, Xi'an City, Shaanxi Province, China.
Abstract
OBJECTIVE: Plasm adiponectin is decreased in smokers. Adiponectin is emerging as a potential key molecular marker in atherosclerosis and other cardiovascular diseases. The aim of this study was to investigate the association between serum adiponectin levels and early atherosclerosis in smokers. Furthermore, the role of the KATP channel in the down-regulation of adiponectin by smoking was preliminarily explored. METHODS: We consecutively enrolled 96 men, including 50 smokers with atherosclerosis and 46 nonsmokers. Serum adiponectin was detected with enzyme-linked immunosorbent assay - in all participants. Large (C1) and small (C2) artery elasticity indices and carotid intima-media thickness (IMT) were measured as evaluation indexes of early atherosclerosis in smokers. Finally, the effect of nicotine via ATP-dependent potassium (KATP) channels on adiponectin secretion by 3T3-L1 preadipocytes was examined in vitro. RESULTS: Adiponectin levels of smokers were statistically negatively correlated to IMT (r = -.440; P < 0.001) and positively correlated to C1 (r = 0.448; P < 0.001) as well as C2 (r = 0.426; P = 0.002). In 3-T3-L1 preadipocytes, nicotine treatment significantly decreased adiponectin levels (P = 0.003), whereas the adiponectin level was rescued by the inhibition of KATP channel (P < 0.001). CONCLUSION: Serum adiponectin level was an independent predictor of early atherosclerosis in smokers. Nicotine might decrease adiponectin in part through altering KATP channels in adipocytes.
OBJECTIVE: Plasm adiponectin is decreased in smokers. Adiponectin is emerging as a potential key molecular marker in atherosclerosis and other cardiovascular diseases. The aim of this study was to investigate the association between serum adiponectin levels and early atherosclerosis in smokers. Furthermore, the role of the KATP channel in the down-regulation of adiponectin by smoking was preliminarily explored. METHODS: We consecutively enrolled 96 men, including 50 smokers with atherosclerosis and 46 nonsmokers. Serum adiponectin was detected with enzyme-linked immunosorbent assay - in all participants. Large (C1) and small (C2) artery elasticity indices and carotid intima-media thickness (IMT) were measured as evaluation indexes of early atherosclerosis in smokers. Finally, the effect of nicotine via ATP-dependent potassium (KATP) channels on adiponectin secretion by 3T3-L1 preadipocytes was examined in vitro. RESULTS:Adiponectin levels of smokers were statistically negatively correlated to IMT (r = -.440; P < 0.001) and positively correlated to C1 (r = 0.448; P < 0.001) as well as C2 (r = 0.426; P = 0.002). In 3-T3-L1 preadipocytes, nicotine treatment significantly decreased adiponectin levels (P = 0.003), whereas the adiponectin level was rescued by the inhibition of KATP channel (P < 0.001). CONCLUSION: Serum adiponectin level was an independent predictor of early atherosclerosis in smokers. Nicotine might decrease adiponectin in part through altering KATP channels in adipocytes.