Page - (000159) - in Biomedical Chemistry: Current Trends and Developments

associated (Chatterjee, 2011). 2.3.6 Bicarbonate and MetSyn/MetSyn Features – Associated Mechanisms In fact, besides calcium, magnesium and potassium content on natural mineral-rich waters, hydrogen carbonate concentration also deserves attention. Hydrogen carbonate-rich mineral waters may decrease calcium and magnesium renal excretion (by increasing their renal reabsorption) and, so, contribute to minerals´ homeostasis in the body (Brandolini, 2005; Rylander, 2008). Water pH and water hydrogen carbonate content are particularly relevant when considering the increased acid load of the Western diet, mainly related to the: a) high- ingestion of proteins (especially from animal origin), since sulfur ions are formed during amino acids metabolism, as well as high-sodium chloride consumption, and b) low-ingestion of fresh fruit, vegetables, tubers, roots and nuts, that are net base producers. As a result, the consumption of a Western diet induces a chronic, low-grade metabolic acidosis that worsens with the decline of kidney function, for example with aging (Cordain, 2005; Rylander, 2008; Zhang, 2009; Adeva, 2011). In line, it was observed that renal sulfate excretion negatively correlates with urine pH and is higher in insulin resistance versus normal insulin sensitivity, highlighting an association among (animal) protein ingestion, endogenous acid production and insulin resistance. Furthermore, insulin resistance has been linked with metabolic acidosis markers (such as low urine pH and low serum bicarbonate levels) (Adeva, 2011). Metabolic acidosis may induce insulin resistance by impairing the insulin signaling pathway through inhibition of PI3K activity and, consequently, of its downstream effectors, in the skeletal muscle (Franch, 2004; Adeva, 2011). This gives dietary acid load a solid role in anticipating the metabolic dysfunction and the cardiovascular risk of the healthy, overweight and obese individuals as well as diabetic, hypertensive and chronic kidney failure patients (Zhang, 2009; Adeva, 2011; Odermatt, 2011). Moreover, acidosis-induced inhibition of PI3K