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

Abstract

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.

Effects of Artemisia dracunculus Aqueous Extract on Blood Sugar, Serum Insulin, Triglyceride and Liver Enzymes in Fructose Drinking Water Male Rats

“…Metabolic syndrome is described the group of character of quite a lot of metabolic abnormalities, based on hyperlipidemia, abdominal obesity and insulin resistance [2]. This disorder is accompanied with an increase in serum insulin, leptin hormone and the possibility for atherosclerotic cardiovascular disease and type 2 diabetes mellitus [3]. Research indicated that in fructose-fed rats (FFR) circulating triglyceride, the weight of liver, abdominal adipose tissue, and insulin resistance (IR) increased that was accompanied with impaired glucose tolerance [4].…”

Natural mineral-rich water ingestion improves hepatic and fat glucocorticoid-signaling and increases sirtuin 1 in an animal model of metabolic syndrome

“…After a 10-day acclimatization period, animals were randomly divided into three groups (seven animals each) with free access to pellet food and different drinking solutions, for 8 weeks: a) tap water (CONT), b) 10% fructose in tap water (FRUCT) or c) 10% fructose in natural mineral-rich water (FRUCTMIN). A 3-week pretreatment period with the natural mineral-rich water was performed to the FRUCTMIN group (while the other rats drank tap water) to allow adjustment to water flavor and sparkles [10,12].…”

“…The chemical characteristics of tap and natural mineral-rich waters are already described [10,12]. The latter [classified as a hypersaline sodium-rich naturally sparkling mineral water in conformity with the European Community Council guidelines for natural mineral waters (2009/54/EEC)] has high total mineralization content (2855 mg/L), is mainly rich in sodium and bicarbonate, and has a higher potassium, calcium and magnesium content than the former.…”

“…In this regard, natural mineral-rich waters can be good sources of highly bioavailable minerals [6]. biochemical approaches, that a hypersaline sodium-rich naturally sparkling mineral water plays a role in the protection against metabolic syndrome (MetSyn) induction in fructose-fed Sprague-Dawley rats [7][8][9][10], a well-characterized MetSyn animal model [11]. Additionally, in the same animal model, this natural mineral-rich water confers protection against endothelial dysfunction in a pattern similar to what is observed in rats subjected to energy restriction or treated with polyphenol-rich beverages protective against MetSyn [12].…”

In vitro ACE-inhibitory peptide KGYGGVSLPEW facilitates noradrenaline release from sympathetic nerve terminals: Relationship with the lack of antihypertensive effect on spontaneous hypertensive rats

“…To minimize stress-induced variations only data from the last 10 min from each 30 min were average for analysis. If difference between SBP and DBP fell below 20 mmHg and/or HR rose above 350 beats/min, blood pressure measurements were considered unreliable [17]. To withdraw the effect of movement in blood pressure measurements, data was only used when locomotor activity in the animal cage was blunted.…”