High salt intake fails to enhance plasma adiponectin in normotensive salt-sensitive subjects

• Published in: Nutrition (Burbank, Los Angeles County, Calif.) Los Angeles County, Calif.), 2012-04, Vol.28 (4), p.422-425
• Main Authors: Liu, Fuqiang, Ph.D, Mu, Jianjun, Ph.D., M.D, Yuan, Zuyi, Ph.D., M.D, Wu, Guanji, M.Sc, Liu, Enqi, Ph.D, Zheng, Shuhui, M.D, Lian, Qiufang, M.D, Ren, Keyu, M.Sc, Xu, Haixia, M.Sc
• Format: Article
• Language: English
• Subjects: Adiponectin; Adiponectin - blood; Adult; Biological and medical sciences; Blood pressure; Blood Pressure - physiology; C-reactive protein; C-Reactive Protein - metabolism; Cardiovascular disease; Chemokine CCL2 - blood; China; Cholesterol; Diet; Diet, Sodium-Restricted; Feeding. Feeding behavior; Female; Fundamental and applied biological sciences. Psychology; Gastroenterology and Hepatology; Humans; Hypertension; Hypertension - blood; Hypertension - physiopathology; Inflammation; Inflammation - chemically induced; Inflammation Mediators - metabolism; Kinases; low sodium diet; Male; Middle Aged; Normotensive; Plasma; Proteins; Reference Values; Rodents; Rural areas; rural communities; Rural Population; salt tolerance; Salts; Sodium chloride; Sodium Chloride, Dietary - adverse effects; Sodium dependent; Studies; Tumor Necrosis Factor-alpha - blood; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 0899-9007; 1873-1244
• DOI: 10.1016/j.nut.2011.08.018

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.