title: Long-term dietary sodium restriction increases adiponectin expression and ameliorates the proinflammatory adipokine profile in obesity.
abstract: OBJECTIVE
  Obesity is associated with changes in adiponectin and pro-inflammatory adipokines. Sodium intake can affect adipokine secretion suggesting a role in cardiovascular dysfunction. We tested if long-term dietary sodium restriction modifies the expression of adiponectin and ameliorates the pro-inflammatory profile of obese, diabetic mice.
  
  
  RESULTS
  Db/db mice were randomized to high sodium (HS 1.6% Na+, n = 6) or low sodium (LS 0.03% Na+, n = 8) diet for 16 weeks and compared with lean, db/+ mice on HS diet (n = 8). Insulin levels were 50% lower in the db/db mice on LS diet when compared with HS db/db (p < 0.05). LS diet increased cardiac adiponectin mRNA levels in db/db mice by 5-fold when compared with db/db mice on HS diet and by 2-fold when compared with HS lean mice (both p < 0.01). LS diet increased adiponectin in adipose tissue compared with db/db mice on HS diet, achieving levels similar to those of lean mice. MCP-1, IL-6 and TNF-α expression were reduced more than 50% in adipose tissue of db/db mice on LS diet when compared with HS db/db mice (all p < 0.05), to levels observed in the HS lean mice. Further, LS db/db mice had significantly reduced circulating MCP-1 and IL-6 levels when compared with HS db/db mice (both p < 0.01).
  
  
  CONCLUSIONS
  In obese-diabetic mice, long-term LS diet increases adiponectin in heart and adipose tissue and reduces pro-inflammatory factors in adipose tissue and plasma. These additive mechanisms may contribute to the potential cardioprotective benefits of LS diet in obesity-related metabolic disorders.
authors.affiliation: Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA; Department of Endocrinology, School of Medicine, Pontificia Universidad Catolica de Chile, Santiago 8330074, Chile.
authors.forename: R
authors.initials: R
authors.lastname: Baudrand
authors.affiliation: Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA; Division of Dermatopathology, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
authors.forename: C G
authors.initials: CG
authors.lastname: Lian
authors.affiliation: Department of Medicine, University of Massachusetts, Worcester, MA 01605, USA.
authors.forename: B Q
authors.initials: BQ
authors.lastname: Lian
authors.affiliation: Department of Pathology and Medicine, University of Cincinnati, Cincinnati, OH 45219, USA.
authors.forename: V
authors.initials: V
authors.lastname: Ricchiuti
authors.affiliation: Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA.
authors.forename: T M
authors.initials: TM
authors.lastname: Yao
authors.affiliation: Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA.
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.affiliation: Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA.
authors.forename: G H
authors.initials: GH
authors.lastname: Williams
authors.affiliation: Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA. Electronic address: gadler@partners.org.
authors.forename: G K
authors.initials: GK
authors.lastname: Adler
mesh_terms: D054392:Adipokines / Q000097:blood / Q000378:metabolism; D052242:Adiponectin / Q000097:blood*; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D018932:Chemokine CCL2 / Q000097:blood; D003920:Diabetes Mellitus / Q000178:diet therapy*; D004032:Diet; D004039:Diet, Sodium-Restricted; D006321:Heart / Q000502:physiology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D007371:Interferon-gamma / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D051379:Mice; D008820:Mice, Obese; D009765:Obesity / Q000097:blood; D012982:Sodium, Dietary / Q000008:administration & dosage*; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D054392:Adipokines; D052242:Adiponectin; D001786:Blood Glucose; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D007328:Insulin; D015850:Interleukin-6; D012982:Sodium, Dietary; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma
keywords: Adiponectin; Diabetes; Inflammation; Insulin resistance; Obesity; Sodium intake