Abstract
Östberg 1 proposed an hypothesis that, in human metabolism, the citrates of the urine constitute one of the important buffer systems. This suggestion evoked considerable investigation relative to the possible function of citric acid as a “metabolic acid” in much the same sense that ammonia is a “metabolic base.” This theory has been supported by the establishment of the endogenous origin of citric acid, as shown by its synthesis in the animal organism from various precursors. 2 , 3 Further-more, when citric acid is administered as the free acid to human subjects 4 , 5 , 6 , 7 , 8 and to experimental animals 9 , 10 , 11 , 12 , 13 , 14 it disappears as such, whereas the ingestion of sodium citrate leads to the appearance of relatively large amounts of citric acid in the urine. 1 , 7 , 9 That this difference is due principally to the alkali administered is indicated by the fact that equivalent amounts of sodium, as the bicarbonate, produce similar increase in citric acid excretion. 1 , 4 , 5 , 6 , 7 , 9 Conversely, the administration of hydrochloric acid and potentially acidic substances, such as ammonium chloride, cause a significant decrease in the excretion of the acid. 1 , 4 , 5 It is evident from these investigations that the endogenous production of citric acid is highly responsive to factors known to affect the recognized metabolic adjustments to changes in acid base equilibrium in the body.
In view of the evidence relative to the qualitative stimulation of citric acid production by alkali, research was inaugurated in an attempt to establish a possible direct relationship between the excretion of citric acid and the amount of alkali administered. Seven male albino rats, weighing from 200-250 g, were maintained over the experimental period on either of 2 low-citrate, iso-caloric diets. Diet Cbh contained Lactalbumin (Labco, No. 15-42, Borden) 14.0%, Dextrin 58.6%, Hy-drogenated Fat (Crisco) 20%, Cod Liver Oil (Mead, Johnson & Company) 5%, Salt Mixture 15 2.4%, while diet Pr consisted of Lactalbumin
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