Natural mineral-rich water ingestion by ovariectomized fructose-fed Sprague-Dawley rats: effects on sirtuin 1 and glucocorticoid signaling pathways.

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 (11ßHSD1). 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 11ßHSD1 (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 11ßHSD1 (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.

Relevance of a Hypersaline Sodium-Rich Naturally Sparkling Mineral Water to the Protection against Metabolic Syndrome Induction in Fructose-Fed Sprague-Dawley Rats: A Biochemical, Metabolic, and Redox Approach.

The Metabolic Syndrome increases the risk for atherosclerotic cardiovascular disease and type 2 Diabetes Mellitus. Increased fructose consumption and/or mineral deficiency have been associated with Metabolic Syndrome development. This study aimed to investigate the effects of 8 weeks consumption of a hypersaline sodium-rich naturally sparkling mineral water on 10% fructose-fed Sprague-Dawley rats (Metabolic Syndrome animal model). The ingestion of the mineral water (rich in sodium bicarbonate and with higher potassium, calcium, and magnesium content than the tap water used as control) reduced/prevented not only the fructose-induced increase of heart rate, plasma triacylglycerols, insulin and leptin levels, hepatic catalase activity, and organ weight to body weight ratios (for liver and both kidneys) but also the decrease of hepatic glutathione peroxidase activity and oxidized glutathione content. This mineral-rich water seems to have potential to prevent Metabolic Syndrome induction by fructose. We hypothesize that its regular intake in the context of modern diets, which have a general acidic character interfering with mineral homeostasis and are poor in micronutrients, namely potassium, calcium, and magnesium, could add surplus value and attenuate imbalances, thus contributing to metabolic and redox health and, consequently, decreasing the risk for atherosclerotic cardiovascular disease.