title: High salt intake fails to enhance plasma adiponectin in normotensive salt-sensitive subjects.
abstract: OBJECTIVE
  Evidence shows that salt can modulate adiponectin and inflammation levels in normal individuals. Therefore, we hypothesized that abnormalities in adiponectin and inflammation might be the potential mechanism of salt sensitivity. The aim of this study was to investigate whether different alterations of adiponectin and inflammation levels in response to a high-salt intake were exhibited between normotensive salt-sensitive and salt-resistant subjects.
  
  
  METHODS
  Thirty normotensive subjects (25 to 50 y old) were selected from a rural community of northern China. They were sequentially maintained on a normal diet for 3 d at baseline, a low-salt diet for 7 d (NaCl 3 g/d), and then a high-salt diet for 7 d (18 g/d).
  
  
  RESULTS
  Salt sensitivity was diagnosed in 10 subjects who exhibited an increase of at least 10% in mean blood pressure from the low-salt to the high-salt periods. Plasma adiponectin was significantly higher with the high-salt intake than with the low-salt intake (6.1 ± 1.3 versus 7.1 ± 1.7 μg/mL, P = 0.047) in normotensive salt-resistant subjects but not in the normotensive salt-sensitive subjects (6.4 ± 2 versus 5.9 ± 2.1 μg/mL, P = 0.481). The high-salt intake markedly increased plasma tumor necrosis factor-α (P < 0.0001) and monocyte chemoattractant protein-1 (P < 0.0001) in normotensive salt-sensitive and salt-resistant subjects. No signiﬁcant change in plasma high-sensitivity C-reactive protein was observed.
  
  
  CONCLUSIONS
  Our data indicate that the disturbance of adiponectin exists in normotensive salt-sensitive subjects during a high-salt diet, which may be a novel underlying mechanism of salt sensitivity.
authors.affiliation: Department of Cardiovascular Medicine, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Peoples Republic of China.
authors.forename: Fuqiang
authors.initials: F
authors.lastname: Liu
authors.forename: Jianjun
authors.initials: J
authors.lastname: Mu
authors.forename: Zuyi
authors.initials: Z
authors.lastname: Yuan
authors.forename: Guanji
authors.initials: G
authors.lastname: Wu
authors.forename: Enqi
authors.initials: E
authors.lastname: Liu
authors.forename: Shuhui
authors.initials: S
authors.lastname: Zheng
authors.forename: Qiufang
authors.initials: Q
authors.lastname: Lian
authors.forename: Keyu
authors.initials: K
authors.lastname: Ren
authors.forename: Haixia
authors.initials: H
authors.lastname: Xu
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D001794:Blood Pressure / Q000502:physiology*; D002097:C-Reactive Protein / Q000378:metabolism; D018932:Chemokine CCL2 / Q000097:blood; D002681:China; D004039:Diet, Sodium-Restricted; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology; D007249:Inflammation / Q000139:chemically induced*; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D012424:Rural Population; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D052242:Adiponectin; D018932:Chemokine CCL2; D018836:Inflammation Mediators; D017673:Sodium Chloride, Dietary; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein