title: Dietary salt restriction improves cardiac and adipose tissue pathology independently of obesity in a rat model of metabolic syndrome.
abstract: BACKGROUND
  Metabolic syndrome (MetS) enhances salt sensitivity of blood pressure and is an important risk factor for cardiovascular disease. The effects of dietary salt restriction on cardiac pathology associated with metabolic syndrome remain unclear.
  
  
  RESULTS
  We investigated whether dietary salt restriction might ameliorate cardiac injury in DahlS.Z-Lepr(fa)/Lepr(fa) (DS/obese) rats, which are derived from a cross between Dahl salt-sensitive and Zucker rats and represent a model of metabolic syndrome. DS/obese rats were fed a normal-salt (0.36% NaCl in chow) or low-salt (0.0466% NaCl in chow) diet from 9 weeks of age and were compared with similarly treated homozygous lean littermates (DahlS.Z-Lepr(+)/Lepr(+), or DS/lean rats). DS/obese rats fed the normal-salt diet progressively developed hypertension and showed left ventricular hypertrophy, fibrosis, and diastolic dysfunction at 15 weeks. Dietary salt restriction attenuated all of these changes in DS/obese rats. The levels of cardiac oxidative stress and inflammation and the expression of cardiac renin-angiotensin-aldosterone system genes were increased in DS/obese rats fed the normal-salt diet, and dietary salt restriction downregulated these parameters in both DS/obese and DS/lean rats. In addition, dietary salt restriction attenuated the increase in visceral adipose tissue inflammation and the decrease in insulin signaling apparent in DS/obese rats without reducing body weight or visceral adipocyte size. Dietary salt restriction did not alter fasting serum glucose levels but it markedly decreased the fasting serum insulin concentration in DS/obese rats.
  
  
  CONCLUSIONS
  Dietary salt restriction not only prevents hypertension and cardiac injury but also ameliorates insulin resistance, without reducing obesity, in this model of metabolic syndrome.
authors.affiliation: Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan (T.H., T.M., M.T., K.N., N.M., S.W., K.N.).
authors.forename: Takuya
authors.initials: T
authors.lastname: Hattori
authors.affiliation: Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan (T.H., T.M., M.T., K.N., N.M., S.W., K.N.).
authors.forename: Tamayo
authors.initials: T
authors.lastname: Murase
authors.affiliation: Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan (T.H., T.M., M.T., K.N., N.M., S.W., K.N.).
authors.forename: Miwa
authors.initials: M
authors.lastname: Takatsu
authors.affiliation: Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan (T.H., T.M., M.T., K.N., N.M., S.W., K.N.).
authors.forename: Kai
authors.initials: K
authors.lastname: Nagasawa
authors.affiliation: Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan (T.H., T.M., M.T., K.N., N.M., S.W., K.N.).
authors.forename: Natsumi
authors.initials: N
authors.lastname: Matsuura
authors.affiliation: Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan (T.H., T.M., M.T., K.N., N.M., S.W., K.N.).
authors.forename: Shogo
authors.initials: S
authors.lastname: Watanabe
authors.affiliation: Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan (T.M.).
authors.forename: Toyoaki
authors.initials: T
authors.lastname: Murohara
authors.affiliation: Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan (T.H., T.M., M.T., K.N., N.M., S.W., K.N.).
authors.forename: Kohzo
authors.initials: K
authors.lastname: Nagata
mesh_terms: D000367:Age Factors; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D006332:Cardiomegaly / Q000097:blood / Q000235:genetics / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D004039:Diet, Sodium-Restricted; D004195:Disease Models, Animal; D005355:Fibrosis; D006439:Hemodynamics; D006973:Hypertension / Q000097:blood / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000378:metabolism / Q000473:pathology*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000178:diet therapy* / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009765:Obesity / Q000097:blood / Q000178:diet therapy* / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D018384:Oxidative Stress; D020303:Rats, Inbred Dahl; D011924:Rats, Zucker; D012084:Renin-Angiotensin System; D017673:Sodium Chloride, Dietary; D013997:Time Factors
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D018836:Inflammation Mediators; D007328:Insulin; D017673:Sodium Chloride, Dietary
keywords: diet; hypertension; obesity; remodeling; sodium