162 III. OXIDATION AND METABOLISM 



conflicting. Although Bennett et al}^>^ noted that ACTH produced an 

 increased ketonemia in a fasted normal dog, and that it also augmented 

 the concentration of ketone bodies in the blood of the fasted rat, and the 

 rate of their excretion in the urine,^''- Kinsell and associates'"^ obtained 

 diametrically opposed results in tests of human subjects. Thus, it was 

 found that the injection of either ACTH or cortisone into most fasting 

 individuals resulted in a partial or complete suppression of the hyper- 

 ketonemia and ketonuria induced by fasting. According to the above 

 workers, these results may be interpreted to mean either that adrenal 

 steroids increase the rate of utilization of ketones by peripheral tissues, 

 that they decrease the rate of formation of ketone bodies from fatty acids, 

 and at the same time increase the rate of direct utilization of fatty acids for 

 energy purposes by peripheral tissues, or finally that certain adrenal 

 steroids so change the metabolic pathway of fatty acids that mid-zone 

 metabolites other than ketones originate. Hexose is suggested as a 

 possible metabolite. 



On the other hand, adrenalectomy reduces or abolishes the ketosis of 

 fasting,'*^' that resulting from pancreatectomy'"* or from phlorhizin,'"' 

 that occurring in pregnancy,'"^ as well as that resulting from the injection 

 of the ketogenic hormone of the anterior pituitary, when determined by the 

 degree of ketonuria.*^' MacKay and Barnes'"^ interpreted the results of 

 their tests, in which they found a lower exogenous ketonuria in adrenalecto- 

 mized than in normal animals, as indicative of the fact that an increased 

 level of ketolysis obtains following the removal of the adrenal glands. 

 This is in line with the results of Bondy and Wilhelmi,*^^ which demon- 

 strated in the case of rat liver slices that adrenalectomy did not reduce 

 the rate of ketogenesis, although in the later periods it did prevent the 

 normal increase in blood ketones. At this later stage, a decrease in the 

 rate of ketogenesis by liver slices did occvir. 



Although Butts et a/.^^^ observed no increased ketonuria in the intact 

 rat when antuitrin was given, Pittoni and Rossi'"^ reported an increased 



601 L. L. Bennett, J. F. Garcia, and C. H. Li, Proc. Soc. Exptl. Biol. Med., 69, 52-53 

 (1948). 



502 L. L. Bennett, R. E. Kreiss, C. H. Li, and H. M. Evans, Am. J. Physiol, 152, 

 210-215(1948). 



"03 L. W. Kinsell, S. Margen, G. D. Michaels, R. Reiss, R. Frantz, and J. Carbone, 

 /. Clin. Invest., 30, 1491-1502 (1951). 



^04 C. N. H. Long and F. D. Lukens, Proc. Soc. Exptl. Biol. Med., 32, 7'^3-745 (1935). 



505 G. Evans, Am. J. Physiol, 114, 297-308 (1936). 



506 E. M. MacKay and R. H. Barnes, Proc. Soc. Exptl Biol Med., 34, 682-G83 (1936). 



507 E. M. MacKay and R. H. Barnes, Ajh. J. Physiol, 122, 101-104 (1938). 



508 A. Pittoni and C. R. Rossi, Bull soc. chim. biol, 33, 1025-1031 (1951). 



