Jane A. Russell ^ 1 1 



pophysectomized cats/" but in these cases the changes occur more slowly than 

 in rats. In the fasted hypophysectomized rat the abnormal loss of muscle 

 glycogen can be prevented entirely by APE administration and the RQ is 

 depressed to normal at the same time.^ " '- This action— the maintenance of 

 fasting muscle-glycogen levels in hypophysectomized animals— has been de- 

 fined as the glycostatic effect, and it can be used to assay APE. The term is 

 also sometimes applied to the effects of APE on liver- and blood-carbohydrate 

 levels, in normal as well as in hypophysectomized animals, but, as will be 

 evident later, these data do not always afford trustworthy evidence of glyco- 

 static activity. 



Two possible explanations exist for the apparent rapid rate of disappear- 

 ance of carbohydrate in the absence of the pituitary and its prevention by 

 APE. One is, of course, that the rate of oxidation of carbohydrate is increased. 

 The other is that, since ordinarily the carbohydrate levels are maintained 

 during fasting by gluconeogencsis, interruption in this process occurs in hy- 

 pophysectomized animals and a normal rate of peripheral oxidation permits 

 the apparently more rapid disappearance of carbohydrate. However, there is 

 not a sufficient fall in the rate of excretion of nitrogen after hypophysectomy 

 in the rat to make a critical difference in gluconeogencsis probable. In addi- 

 tion, data obtained from experiments on rats fed glucose and on eviscerated 

 animals indicate that an accelerated rate of peripheral oxidation of carbo- 

 hydrate exists in the hypophysectomized animal. 



One of the first, but still most convincing, of these experiments was one in 

 which hypophysectomized and normal rats, after being fasted, were fed meals 

 of carbohydrate (starch) and the glycogen and blood-sugar values followed 

 for 36 hours thereafter. It was found that the hypophysectomized rats could 

 be fed twice as much carbohydrate as the normal rats and at the end of the 

 experimental periods still have much lower levels of liver and muscle glycogen 

 than the control animals. That is, despite metabolic rates one-third below 

 normal, the hypophysectomized rats must have disposed of twice as much 

 carbohydrate as the normal animals in the given time.' Further demonstration 

 of the increased rate at which hypophysectomized animals dispose of carbo- 

 hydrate is seen, together with an indication of its fate, in balance studies of 

 the Cori type (table i).'" In this case, a much smaller proportion of the 

 absorbed glucose was reco\ered 4 hours after its feeding in the hypophysec- 

 tomized rat than in the normal, and respiratory data obtained during the 

 absorption period indicated that the carbohydrate which disappeared could 

 have been oxidized. Now if one is to explain the difference between the find- 

 ings in the normal and the hypophysectomized rats on the basis only of a 

 decrease in gluconeogencsis in the latter case, then one would have to assume 

 that massive gluconeogencsis had taken place in the normal animals under 

 these conditions— in an amount equal to about half of the carbohydrate de- 

 posited—in the presence of a plethora of carbohydrate. 



