title: Elevating circulation chemerin level is associated with endothelial dysfunction and early atherosclerotic changes in essential hypertensive patients.
abstract: OBJECTIVE
  Chemerin is a new adipokine elevated in states of obesity and metabolic syndromes. In this study, we investigated the association of increased chemerin on endothelial function, arterial stiffness and early atherosclerosis in essential hypertensive patients.
  
  
  METHODS
  Three hundred and sixty-seven newly diagnosed essential hypertensive patients were enrolled. Anthropometric measurements and plasma parameters were examined, including BMI, waist circumference, glucose, serum insulin, lipid profiles, chemerin, high-sensitivity C-reactive protein, tumor necrosis factor-α, and interleukin-4. Vascular health was assessed with brachial flow-mediated dilatation (FMD), brachial-ankle pulse wave velocity (baPWV), and carotid intima-media thickness (IMT).
  
  
  RESULTS
  In hypertensive patients, plasma chemerin levels were higher in women than in men (P < 0.05). In univariate analysis, the plasma chemerin level was positively correlated with baPWV (men: r = 0.58, P < 0.01; women: r = 0.51, P < 0.01) and carotid IMT (men: r = 0.17, P = 0.01; women: r = 0.20, P = 0.01), and inversely correlated with FMD (men: r = -0.54, P < 0.01; women: r = -0.44, P < 0.01). The associations for FMD and baPWV, but not IMT, remained significant in multivariable models adjusted for age, sex, glucose homeostasis, lipid profiles, inflammation markers and adipokines. More importantly, logistic regression analysis revealed that high chemerin level was an independent predictor of impaired endothelial function (FMD odds ratio 1.58, 95% confidence interval 1.28-3.30, P = 0.03) and increased arterial stiffness (baPWV odds ratio 3.75, 95% confidence interval 1.36-5.28, P < 0.01), even after adjustment for metabolic variables, inflammatory markers and adipokines.
  
  
  CONCLUSIONS
  Chemerin levels were independently associated with the index of arterial function and early atherosclerosis in essential hypertension.
authors.affiliation: aDepartment of Endocrinology, Jinling Hospital/Nanjing General Hospital of Nanjing Military Command, Nanjing University School of Medicine, Nanjing, Jiangsu Province bDepartment of Neurology, the 309th Hospital of Chinese People's Liberation Army, Beijing, P.R. China cState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong S. A. R. dDepartment of Cardiology, Jiangsu Provincial Hospital of Traditional Chinese Medicine, Nanjing eJinling Hospital/Nanjing General Hospital of Nanjing Military Command, Nanjing University School of Medicine, Nanjing, Jiangsu Province, P.R. China *Ping Gu, Maowei Cheng, and Xiaoyan Hui contributed equally to the writing of this article.
authors.forename: Ping
authors.initials: P
authors.lastname: Gu
authors.forename: Maowei
authors.initials: M
authors.lastname: Cheng
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Hui
authors.forename: Bin
authors.initials: B
authors.lastname: Lu
authors.forename: Weimin
authors.initials: W
authors.lastname: Jiang
authors.forename: Zhaorong
authors.initials: Z
authors.lastname: Shi
mesh_terms: D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000097:blood* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D059168:Carotid Intima-Media Thickness; D018925:Chemokines / Q000097:blood*; D004727:Endothelium / Q000503:physiopathology*; D000075222:Essential Hypertension; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D063177:Pulse Wave Analysis; D012737:Sex Factors; D059289:Vascular Stiffness
chemical_list: D015415:Biomarkers; D018925:Chemokines; D036341:Intercellular Signaling Peptides and Proteins; C478630:RARRES2 protein, human