Excess casein in the diet is not the unique cause of low-grade metabolic acidosis: role of a deficit in potassium citrate in a rat model

Abstract

This study examined the effects of a dietary model of protein excess and K anion salt deficit on the occurrence of metabolic acidosis in rat. Rats were adapted to diets containing either 13 or 26% casein, together with mineral imbalance, through lowering K/increasing sodium/omitting alkalinizing anions. For each protein level, a group of rats was supplemented with K citrate. Dietary K citrate resulted in neutral urinary pH, whatever the protein level. Urea excretion was higher in rats adapted to 26% casein than 13% casein diets, but K citrate enhanced this excretion and suppressed ammonium elimination. No citraturia could be observed in acidotic rats, whereas K citrate greatly stimulated citraturia and 2-ketoglutarate excretion. In conclusion, low-grade metabolic acidosis can occur with a moderate protein level in the diet. K citrate was apparently less effective in rats adapted to the 26% casein level than in those adapted to the 13% casein level with regard to magnesium, citrate and 2-ketoglutarate concentrations in urine.