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.

Contribution of Various Dietary Constituents to the Acid Base Status: Interest of Animal Models of Latent Metabolic Acidosis

“…In rats, it has been observed that LMA takes place in animals adapted to high (26%) but also in those adapted to a moderate (13%) casein diet, if the mineral moiety of the diet is poorly alkalinizing. On the other hand, the high protein diet acidifying effect was blunted if the diet also contained a sufficient amount of K citrate [9]. This indicates that intake of relatively high levels of protein would not lead to acid-base desequilibrium if accompanied by sufficient amounts of K organic salts, as observed with well-balanced omnivorous diets.…”

“…In these models, high dietary protein levels (from 20 to 48%) were found to elicit a marked rise of urinary net acid excretion, together with a greater calciuria and a severe hypocitraturia. This model was also shown to be responsive to a supplementation of alkalin-ising K salts (malate or citrate) in the diet, which reduced Ca and Mg urine excretion and restored citraturia [9]. Such rodent models are quite useful for studies on the effects of alkalinizing compounds or complex foods on LMA [10] and its consequences, for example on bone status or on the risk of renal lithiasis.…”

“…These treatments generally lead to overt metabolic acidosis with marked alterations of acid-base parameters in blood (in contrast to LMA) and, in addition, NH 4 Cl will interfere with nitrogen metabolism. These considerations prompted studies on the feasability of rat model of LMA by introducing dietary alterations liable to chronically disturb the acid-base balance, namely (i) changes in dietary protein level (hence sulfur AA provision) and/or sulfur amino acid supplementation, (ii) changes in the mineral moiety of the diet, especially the balance between inorganic and organic K salts [8,9] and (iii) strict limitation of alkalinizing anions (carbonate, citrate). In these models, high dietary protein levels (from 20 to 48%) were found to elicit a marked rise of urinary net acid excretion, together with a greater calciuria and a severe hypocitraturia.…”