28o C. N, H. LONG 



In spite of this, it was soon surmised that the control of the electro- 

 lyte or carbohydrate levels did not fully explain the action of the hor- 

 mone. For while it is true that adrenalectomized animals or humans 

 with adrenal insufficiency might die from electrolyte loss or carbo- 

 hydrate depletion, the mere administration of sodium salts or carbohy- 

 drate was not sufficient to return them to a normal state, even though 

 life might b€ extended by their use. 



In 1934 Lukens and I (13) found that adrenalectomy alleviated 

 many of the consequences of total pancreatectomy in the cat and dog. 

 The most notable effect, apart from a prolongation of life, was the 

 reduction in urinary glucose and nitrogen excretion, a fall from the 

 characteristically high to more normal blood glucose levels and a strik- 

 ing abatement of ketosis. 



The general conclusion concerning these metabolic changes was that 

 adrenalectomy reduced the high rate of conversion of tissue proteins 

 to glucose (gluconeogenesis) while at the same time allowed a higher 

 rate of carbohydrate utilization. The converse conclusion would be that 

 the adrenal cortical hormones accelerated the conversion of tissue pro- 

 teins to glucose and/or inhibits carbohydrate utilization by the tissues. 



Later experiments demonstrated that in other conditions accom- 

 panied by a high rate of gluconeogenesis from protein, adrenalectomy 

 was followed by a comparable reduction in the quantity of protein 

 undergoing catabolism. It has since been shown in several laboratories 

 besides our own that the injection of either the cortical steroids or 

 adrenotrophic hormone into normal fasting animals increases the rate 

 of protein breakdown to a marked degree, while at the same time large 

 quantities of glycogen are deposited in the liver. In fed animals, as Ingle 

 has shown, actual glycosuria follows prolonged injection of either of 

 these hormones, indicating that carbohydrate utilization was also sup- 

 pressed. 



The adrenal cortical hormones, by their capacity to accelerate the 

 catabolic phases of protein metabolism, retard the growth of growing 

 animals. They therefore stand in opposition to the growth promoting 

 factor of the pituitary, which promotes the retention of protein in the 

 body. Since the activities of the adrenal cortex are also regulated by 

 the anterior pituitary, this gland exercises control over the rate of both 

 the catabolism and anabolism of protein. 



Though we use such terms as "promotion of gluconeogenesis," "stim- 

 ulation of protein catabolism," and "inhibition of carbohydrate utiliza- 

 tion" to describe the function of the adrenal cortex, we have not yet 



