THE PITUITARY BODY 



60° C, their earlier report (Anselmino, Effkemann, and Hoff- 

 mann, 1935) emphasized that (i) the consistent effect of the 

 extract is an unsaturation of fatty acids of the Hver and (2) 

 the concentration of total fatty acids in the liver falls or 

 rises depending upon the presence of high or low initial 

 levels. •'° 



It must be remembered that, if the concentration of ace- 

 tone bodies in the blood increases or if the urinary excretion 

 of these bodies becomes markedly elevated after the injec- 

 tion of anterior pituitary extract, these facts do not justify 

 naming the causative substance "fat-metabolism hormone." 

 The experimental data indicate that its action depends upon 

 the presence of intact adrenal tissue. Dingemanse (1936) is 

 not convinced that a ketogenic hormone exists and found (i) 

 that only an occasional extract raises the level of acetone 

 bodies in the blood of the rat (but not the rabbit), (2) its 

 detection is difficult because of the effect of fasting, time of 

 day, etc., and (3) the ratio of (3 hydroxybutyric acid to 

 acetoacetic acid and acetone is the same, whether keto- 

 genesis is caused by fasting or by extract. 



Mirsky (1936) takes the position that inasmuch as keto- 

 genesis cannot occur in the absence of the liver, a ketogenic 

 effect depends upon the utilization of non-carbohydrate foods 

 in the absence of ample carbohydrate available for oxidation 

 by the cells of the liver. He prevented the ketogenic action 

 of anterior pituitary extract in rabbits fasted for 24 hours by 

 the injection of insulin (1.3-3 units per kg. body-weight) 

 or ergotamine tartrate (2 mg. per kg. body-weight). Both of 

 these substances were considered to prevent glycogenolysis, 

 thus acting as ketolytic agents. Anselmino and Hoffmann 

 (1936) concluded that insulin inhibits the liberation of a 

 ketogenic hormone occurring otherwise as a result of feeding 

 butter. The authors used dogs. 



3° The same authors (1935) stated that "carbohydrate-metabolism hormone" 

 causes an effect the opposite of (i) and also brings about a fall in the concentration 

 of total fatty acids. 



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