828 PERIODIC FUNCTIONS IN MAMMALS 



corticoid in period A may be a case in point, since information is lack- 

 ing as to how such an oxycorticoid effect is exerted. Oxycorticoids 

 have also been called "sugar hormones" — is their effect upon perio- 

 dicity related to that upon carbohydrate metabolism? Is it exerted 

 upon some phosphorylating step, which need not involve an immediate 

 precursor of phospholipid and which may be relatively independent 

 of phospholipid formation as a whole? Is glycogen deposition in the 

 liver a sine qua non for its rhythmicity? Can we account for the dis- 

 sociation, along the 24-hr scale, of the peaks in hepatic glycogen and 

 blood oxycorticoid simply by feeding time and by suggesting that, for 

 a while after the initiation of feeding, sugar is being used up at a rate 

 comparable to that at which it is being made available? To our knowl- 

 edge there is no critical evidence supporting such views. What are the 

 time relations of blood oxycorticoid and liver glycogen during starva- 

 tion, while these rhythms persist? A partial answer to these questions 

 may, perhaps, be obtained from studies of ( 1 ) the sequence in which 

 the various peaks of periodic cellular events are altered by adrenal- 

 ectomy, and of (2) the time relation of such alterations to changes in 

 periodic glucose resorption from the gut and gluconeogenesis from 

 protein. 



In 1940 Hamar concluded that the daily variations in glucose re- 

 sorption from the small intestine of rats may result either from the 

 periodic hormone secretion of the adrenal cortex or from periodicity 

 in the sensitivity of the intestinal epithelium to cortical hormones. To- 

 day, his inferences remain timely, even though the data upon which 

 they were based describe "adrenalectomized" rats probably possessing 

 ectopic cortical tissue, a circumstance stated by Hamar. It is further 

 pertinent that by 1935, Agren had reported that the rhythm in liver 

 glycogen was not demonstrable in adrenalectomized rats. This author, 

 in turn, suggests that he dealt with true cortical adrenal insufficiency; 

 the extremely low or zero values which he recorded for liver glycogen 

 in most of his rats may be used to support his conclusion for this 

 majority of his animals. Agren's data have recently been recomputed, 

 however, as relative curves, by Sollberger ( 1955a, b) who comments 

 on the surprising similarity of the rhythms in liver glycogen of starved 

 and adrenalectomized rats. In relative curves, changes are expressed 

 as percent of series mean, e.g., for the purpose of eliminating undue 



