524 Pituitary and Carbohydrate Metabolism 



view that the adrenocorticotrophic factor is the glycostatic substance. It 

 is not siuprising that adrenocorticotrophic and cortical hormones should 

 counteract the action of insiUin, for their gluconeogenetic action might be 

 compared almost to that of the administration of glucose in preventing insulin 

 convulsions. It is important, however, that complete parallelism between 

 adrenocorticotrophic and anti-insulin activities has not yet been demonstrated 

 in all APE. That is, there may still be other anti-insulin factors in APE than 

 adrenocorticotrophic hormone, and this may be expected from the frequent 

 observations of glycotrophic activity in the crudest of APE, which ordinarily 

 contain little adrenocorticotrophic hormone. There is also evidence that an 

 anti-insulin factor in APE acts in the absence of the adrenals, for Himsworth 

 and Scott"' report the full glycostatic activity of APE in adrenalectomized 

 rabbits. While the activity of the adrenal cortex must be very important in 

 determining an animal's response to insulin, it is not certain that the hyper- 

 sensitivity to insidin after hypophysectomy and the glycotrophic action of 

 APE are in fact solely the result of their relationship to the adrenal cortex. 



Turning from the fasted animal to that fed carbohydrate, we find further 

 evidence that the hypophysis and the adrenal cortex have different fiuictions. 

 Now both cortin and APE (the former given in quite large amounts, however) 

 depress the oxidation and increase storage of the fed carbohydrate."'' ^' One dif- 

 ference between these actions is apparent, however: APE promotes the deposi- 

 tion in muscle exclusively, whereas cortin causes deposition principally in 

 the liver and to a smaller extent in the muscles of normal animals. In adrenal- 

 ectomized rats, this difference was more clearly seen: cortical hormone did 

 not increase deposition in the periphery at all, but only in the liver. In 

 addition, there is another curious feature of these relationships: in adrenal- 

 ectomized rats the APE alone failed to have any effect on oxidation and 

 only a small effect on muscle-glycogen deposition at the expense of liver 

 glycogen. When, however, cortin was given along with APE, there occurred 

 the usual unique effect of APE on muscle-glycogen deposition at the expense 

 of oxidation. This effect of cortin occurs even when the amount of cortin 

 given is too small to have any effect by itself.'" There is apparently a sort of 

 synergism here between the APE and the cortical hormone; the relationship 

 is not exclusively trophic, for the presence of acting cortical tissue is not neces- 

 sary for the action of the APE, nor is the presence of cortical hormone in any 

 large amount— only enough is required to "grease the wheels," so to speak. This 

 phenomenon has also been observed elsewhere in hypophysectomized rats, 

 and it was observed by Long in adrenalectomized-depancreatized rats, in 

 which, when cortin was given, APE, without effect by itself, was now able to 

 produce a further increase in the glycosuria.^ 



Whether the cortical and anterior pituitary hormones repress carbohydrate 

 oxidation by the same mechanisms or not is unknown. Since quite large 

 amounts of cortical hormone are required to produce these effects, in con- 



