The Effect of Various Organs on the Acetone Content of the Blood in Phlorhizin and Pancreatic Diabetes

Inasmuch as the accumulation of acetone bodies in the blood of a diabetic animal may exert a toxic influence, the study of acetone metabolism has been the subject of numerous investigations. The early observations made on surviving organs indicated that the perfusion of the liver with the amino acids, leucine, phenylalanine, or tyrosine caused an increased acetone content of the perfusate (Embden, Salomon, and Schmidt, 1906; Embden and Oppenheimer, 1912; Masuda, 1912; Loeb, 1914). That the liver was the only source of acetone bodies was concluded from experiments on excised tissue which was perfused with the animal’s own blood (Ahnagia and Embden, 1905 ; Embden and Kalberlah, 1906). The conversion of part of the fi-hydroxybutyric acid of the perfusing fluid of the liver to acetoacetic acid was noted by Snapper and Griinbaum (1927). However, neither compound was oxidized in the liver. Acetoacetic acid injected into normal and depancreatized dogs remained longer in the blood of the depancreatized animals despite the fact that the muscles of both types of experimental animals utilized acetone with equal facility (Chaikoff and Soskin, 1928-29). The authors concluded that the liver of the depancreatized dog produced acetone bodies. In the present study of phlorhizinized and depancreatized dogs an attempt was made to determine the effects of the various organs by analyses of samples of their afferent and efferent blood for acetone bodies.