title: High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome.
abstract: OBJECTIVE
  High sodium (HS) diet is associated with hypertension (HT) and insulin resistance (IR). We evaluated whether HS diet was associated with a dysregulation of cortisol production and metabolic syndrome (MetS).
  
  
  METHODS
  We recruited 370 adults (18-85 years, BMI 29·3 ± 4·4 kg/m(2) , 70% women, 72% HT, 61% MetS). HS diet (urinary sodium >150 mEq/day) was observed in 70% of subjects. We measured plasma hormones, lipid profile, urinary free cortisol (UFC) and cortisol tetrahydrometabolites (THM).
  
  
  RESULTS
  Urinary sodium was correlated with UFC (r = +0·45, P < 0·001), cortisol THM (r = +0·41, P < 0·001) and inversely with adiponectin, HDL and aldosterone, after adjusting by age, gender and BMI. Subjects with high, compared with adequate sodium intake (50-149 mEq/day) had higher UFC (P < 0·001), THM (P < 0·001), HOMA-IR (P = 0·04), HT (81% vs 50%, P < 0·001), MetS (69% vs 41%, P < 0·001) and lower adiponectin (P = 0·003). A multivariate predictive model adjusted by confounders showed a high discriminative capacity for MetS (ROC curve 0·878) using four clinical variables: HS intake [OR = 5·6 (CI 2·3-15·3)], HOMA-IR [OR 1·7 (1·3-2·2)] cortisol THM [OR 1·2 (1·1-1·4)] and adiponectin [OR = 0·9 (0·8-0·9)], the latter had a protective effect.
  
  
  CONCLUSIONS
  High sodium diet was associated with increased urinary cortisol and its metabolites. Also, HS diet was associated with HT, insulin resistance, dyslipidaemia and hypoadiponectinaemia, even when adjusting by confounding variables. Further, we observed that high salt intake, IR and higher cortisol metabolites, alone or combined in a clinical simple model, accurately predicted MetS status, suggesting an additive mechanism in obesity-related metabolic disorders.
authors.affiliation: Department of Endocrinology, School of Medicine, Pontificia Universidad Catolica de Chile, Santiago, Chile; Millennium Institute of Immunology and Immunotherapy, Pontificia Universidad Catolica de Chile, Santiago, Chile.
authors.forename: R
authors.initials: R
authors.lastname: Baudrand
authors.forename: C
authors.initials: C
authors.lastname: Campino
authors.forename: C A
authors.initials: CA
authors.lastname: Carvajal
authors.forename: O
authors.initials: O
authors.lastname: Olivieri
authors.forename: G
authors.initials: G
authors.lastname: Guidi
authors.forename: G
authors.initials: G
authors.lastname: Faccini
authors.forename: P A
authors.initials: PA
authors.lastname: Vöhringer
authors.forename: J
authors.initials: J
authors.lastname: Cerda
authors.forename: G
authors.initials: G
authors.lastname: Owen
authors.forename: A M
authors.initials: AM
authors.lastname: Kalergis
authors.forename: C E
authors.initials: CE
authors.lastname: Fardella
mesh_terms: D052242:Adiponectin / Q000097:blood; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000450:Aldosterone / Q000652:urine; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D015331:Cohort Studies; D005260:Female; D005938:Glucocorticoids / Q000378:metabolism / Q000652:urine; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism / Q000652:urine*; D006973:Hypertension / Q000453:epidemiology; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000453:epidemiology*; D008875:Middle Aged; D009765:Obesity / Q000453:epidemiology; D016017:Odds Ratio; D012982:Sodium, Dietary / Q000009:adverse effects* / Q000652:urine; D055815:Young Adult
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D005938:Glucocorticoids; D012982:Sodium, Dietary; D000450:Aldosterone; D006854:Hydrocortisone