Prevention or induction of metabolic disorders and obesity depend on estrogen signaling and/or exogenous factors, such as mineral content in diet. The protective effects of a Portuguese natural mineral-rich water against the induction of metabolic syndrome in fructose-fed male Sprague-Dawley rats have been reported. The present study was designed to assess the impact of this mineral-rich water on fructose-fed estrogen-deficient female Sprague-Dawley rats.
Ovariectomized rats had access to tap (TWO) or mineral-rich (MWO) waters, with and without 10% fructose (10-wk treatment). A sham-operated (tap water supplied) group was included and each of the five groups included six rats. Plasma biochemical and metabolic parameters were evaluated by routine clinical measurements. Western blotting was used to assess hepatic protein expression of sirtuins (Sirt) 1 and 3, phosphorylated AMP-activated protein kinase-α (p-AMPKα), peroxisome proliferator-activated receptor gamma coactivator-1-α (PGC1α), glucocorticoid receptor, and 11beta-hydroxysteroid dehydrogenase type 1 (11βHSD1).
Ovariectomy increased plasma total cholesterol (46%/P < 0.05), but had no significant effects on hepatic protein expression. Fructose intake by ovariectomized rats increased PGC1α and 11βHSD1 (fructose in tap water [TWFO] vs TWO: 65%/P < 0.05 and 38%/P = 0.05, respectively) as well as glucocorticoid receptor (TWFO and fructose in natural mineral-rich water [MWFO] vs TWO and MWO: 107%/P = 0.05 and 182%/P < 0.05, respectively). Mineral-rich water ingestion exerted an increasing shape on Sirt1 (MWO vs TWO: 76%/P < 0.05; MWFO vs TWFO: 76%/P = 0.06), PGC1α (MWO vs TWO: 77%/P < 0.01), p-AMPKα (MWO vs TWO: 152%/P = 0.01; MWFO vs TWFO: 107%/P = 0.01), and 11βHSD1 (MWO vs TWO: 91%/P = 0.05; MWFO vs TWFO: 47%/P = 0.05).
Mineral-rich water ingestion may have a prime role on the activation of Sirt1 signaling and the modulation of glucocorticoid signaling in the postmenopause.
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1Department of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal
2School of Biotechnology, KIIT University, Bhubaneswar, India
3Department of Clinical Epidemiology, Predictive Medicine and Public Health, Faculty of Medicine, University of Porto, Porto, Portugal
4Unidade de Investigação em Epidemiologia (EPIUnit), Instituto de Saúde Pública, University of Porto, Porto, Portugal
5Escola Superior de Saúde, Instituto Politécnico de Leiria, Campus 2 - Morro de Lena - Alto do Vieiro, Leiria, Portugal
6Clinical Pathology Department of São João Hospital Centre, Porto, Portugal
7CIAFEL - Research Centre in Physical Activity, Health and Leisure, Faculty of Sport, University of Porto, Porto, Portugal
8Instituto de Investigação e Inovação em Saúde (i3 s), University of Porto, Porto, Portugal
9Department of Experimental Biology, Faculty of Medicine, University of Porto, Porto, Portugal.
Address correspondence to: Jugal Kishore Das, MSc, Department of Biochemistry, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal. E-mail: email@example.com
Received 30 May, 2016
Revised 7 September, 2016
Accepted 7 September, 2016
Funding/support: The study was funded by Fundação para a Ciência e a Tecnologia (project reference: UID/BIM/04293/2013), Erasmus Mundus Euphrates (project reference: 2013-2540/001-001), and Unicer Bebidas, S.A. When considering the partial funding by Unicer Bebidas, S.A., it is important to mention that the study here presented was developed, in its full extent, both in scientific terms and research equipment conditions, independently of this company.
Financial disclosure/conflicts of interest: None reported.
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