title: Natural mineral-rich water ingestion improves hepatic and fat glucocorticoid-signaling and increases sirtuin 1 in an animal model of metabolic syndrome.
abstract: BACKGROUND
  We recently reported protection against metabolic syndrome (MetSyn) induction and endothelial dysfunction by natural mineral-rich water intake in fructose-fed Sprague-Dawley rats. As glucocorticoids are critical to MetSyn development, we aimed to further characterize the beneficial effects of mineral-rich water intake in that animal model, by assessing relevant effectors in glucocorticoid-signaling in liver and subcutaneous (SCAT) and visceral (VAT) adipose tissues, sites with a central role in metabolic (dys)regulation.
  
  
  METHODS
  Adult male rats had free access to standard diet and different drinking solutions (8 weeks): a) tap water (CONT), b) 10% fructose/tap water (FRUCT) or c) 10% fructose/mineral-rich water (FRUCTMIN). 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), glucocorticoid receptor (GR), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α) and sirtuin 1 (Sirt1) tissue protein expressions were evaluated by Western blot. Plasma corticosterone (ELISA) and non-esterified fatty acids (NEFA) levels were quantified spectrophotometrically.
  
  
  RESULTS
  Expectedly, Sirt1 and PGC1-α significantly decreased in liver, 11β-HSD1 tended to increase in VAT and tended to decrease in liver and SCAT, and plasma corticosterone tended to increase in FRUCT vs. CONT. Mineral-rich water showed a trend towards a reduction of these fructose effects and significantly increased hepatic Sirt1 vs. CONT and FRUCT. GR significantly increased in VAT and plasma NEFA strongly tended to increase in FRUCTMIN vs. CONT and FRUCT.
  
  
  CONCLUSIONS
  Glucocorticoid-signaling was different among SCAT and VAT and also in liver. Mineral-rich water modulation of fructose effects on glucocorticoid-signaling and Sirt1 underlines the better metabolic profile found earlier.
authors.forename: Cidália D
authors.initials: CD
authors.lastname: Pereira
authors.forename: Milton
authors.initials: M
authors.lastname: Severo
authors.forename: Delminda
authors.initials: D
authors.lastname: Neves
authors.forename: António
authors.initials: A
authors.lastname: Ascensão
authors.forename: José
authors.initials: J
authors.lastname: Magalhães
authors.forename: João T
authors.initials: JT
authors.lastname: Guimarães
authors.forename: Rosário
authors.initials: R
authors.lastname: Monteiro
authors.forename: Maria João
authors.identifier: http://orcid.org/0000-0002-3560-3261
authors.initials: MJ
authors.lastname: Martins
mesh_terms: D000818:Animals; D004032:Diet; D004195:Disease Models, Animal; D060766:Drinking Water; D005223:Fats / Q000378:metabolism; D005632:Fructose / Q000378:metabolism; D005938:Glucocorticoids / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000188:drug therapy*; D008900:Mineral Waters / Q000627:therapeutic use*; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D056564:Sirtuin 1 / Q000378:metabolism*
chemical_list: D060766:Drinking Water; D005223:Fats; D005938:Glucocorticoids; D008900:Mineral Waters; D005632:Fructose; D056564:Sirtuin 1