Jugal Kishore Das1, Milton Severo, Cidália Dionísio Pereira, Emília Patrício, José Magalhães, Rosário Monteiro, Delminda Neves, Maria João Martins. 1. 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.
Abstract
OBJECTIVE: 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. METHODS: 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). RESULTS: 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). CONCLUSIONS: Mineral-rich water ingestion may have a prime role on the activation of Sirt1 signaling and the modulation of glucocorticoid signaling in the postmenopause.
OBJECTIVE: 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. METHODS: 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). RESULTS: 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). CONCLUSIONS: Mineral-rich water ingestion may have a prime role on the activation of Sirt1 signaling and the modulation of glucocorticoid signaling in the postmenopause.
Authors: Laura Narciso; Andrea Martinelli; Flavio Torriani; Paolo Frassanito; Roberta Bernardini; Flavia Chiarotti; Cinzia Marianelli Journal: Front Nutr Date: 2022-05-24