Seite - (000160) - in Biomedical Chemistry: Current Trends and Developments

activity blocked the antiproteolytic effect of insulin, which could be related to decreased lean body mass in chronic kidney failure patients (Franch, 2004). Metabolic acidosis increases both glucocorticoid secretion and plasma cortisol levels, which definitely contribute to insulin resistance, T2DM, MetSyn, blood pressure and inflammation. Contemporary acidogenic diet associates with cortisol excess, the latter being prevented by bicarbonate administration (Zhang, 2009; Adeva, 2011; Pereira, 2011; Pereira, 2012b; Pereira, 2012c). In this context, once more, natural mineral-rich water consumption would be extremely beneficial. 2.3.7 Magnesium, Calcium, Potassium and Bicarbonate versus Sodium As highlighted above, an adequate intake of magnesium, calcium or potassium has a favorable effect on metabolic regulation and/or blood pressure (Whelton, 1997; Geleijnse, 2005; Karppanen, 2005; Teegarden, 2006; Feldeisen, 2007; Olatunji, 2007; van Meijl, 2008; Cho, 2009; Tremblay, 2009; Chaudhary, 2010; Abete, 2011; Rice, 2011). However, their association, as occurs in the dietary approaches to stop hypertension (DASH diet), which includes, among others, magnesium, calcium and potassium-rich foods, seems more effective, particularly in blood pressure control (Vaskonen, 2003; Al-Solaiman, 2010). Furthermore, magnesium, calcium and potassium reduce sodium retention, which may contribute to their positive effects on blood pressure (Vaskonen, 2003; Rice, 2011). In some studies, sodium chloride is clearly associated with hypertension (Ziomber, 2008; Santos, 2010). This association depends on sodium being accompanied by chloride, as sodium per se (in the drinking solution) does not increase blood pressure (Ziomber, 2008; Santos, 2010). Possibly through sodium potassium ATPase inhibition (Blaustein, 2006), only sodium chloride seems to increase plasma volume and blood pressure (Kunes, 2004; Santos, 2010), although sodium salts, with chloride or other anions (with equimolar amounts of sodium), produce similar suppression of the renin-angiotensin axis (Luft, 1990; Santos, 2010).