2. Endocrines and Populations 209 



back system to maintain homeostasis or to meet emergencies. Nevertheless, 

 much has been learned about the specific activities of these hormones by 

 the classic experimental approaches to such a problem : the substitution of 

 pure hormones or extracts into intact and adrenalectomized animals and 

 refinements of these procedures. The effects of injected carbohydrate-active 

 corticoids are closely paralleled by those produced by injecting adreno- 

 corticotropin (ACTH), the hormonal protein of the anterior pituitary 

 responsible for stimulating the secretion of the carbohydrate-active and 

 Ci9 steroids from the adrenal cortex (Poore and Hollander, 1957; Li et al., 

 1957; Lostroh and Li, 1957; Wilson, et al., 1958; Farrell et al., 1958). 



The carbohydrate-active corticoids stimulate gluconeogenesis from pro- 

 teins, and this activity is reflected by hyperglycemia and glycosuria (Ingle, 

 1949; 1950; Jones, 1957). The increased levels of glucose in the blood and 

 urine are also partly due to the inhibition of glucose utilization (Jones, 

 1957) . These hormones also increase glycogen deposition in the liver by 

 accelerating its formation and depressing its release (Ligle, 1950; Jones, 

 1957) . Glycogen deposition commonly is used to bioassay steroids for their 

 gluconeogenic activity and other effects of carbohydrate metabolism (Dorf- 

 man, 1949). The carbohydrate-active steroids not only increase protein 

 catabolism, but they also depress protein anabolism (Engel, 1952). These 

 two actions on protein metabolism are reflected by an increase in the non- 

 protein nitrogen of the blood as well as an increase in the excretion of uri- 

 nary nitrogen (Selye, 1950) . Lipogenesis is inhibited by the carbohydrate- 

 active corticoids, but their effects on lipid metabolism are poorly understood 

 (Jones, 1957) . There is considerable evidence to indicate that hydrocorti- 

 sone and cortisone increase the sensitivity of blood vessels to the actions of 

 epinephrine and norepinephrine, and that these steroids perform an essen- 

 tial function in maintaining normal tonus of the vasculature (Zweifach 

 et al., 1953; Ramey and Goldstein, 1957). The carbohydrate-active hor- 

 mones also decrease capillary permeability and fragility and antagonize the 

 spreading action of hyaluronidase, presumably by their effects on the 

 ground substance; these corticoids appear to decrease permeability of the 

 ground substance, and their ability to decrease capillary permeability may 

 be dependent on this effect (Seifter et al., 1953; Zweifach et al., 1953). In 

 these effects the carbohydrate-active corticoids are opposed by the actions 

 of the sodium-retaining corticoids and growth hormone (Seifter et al., 1953; 

 Kass et al. 1953b; Dougherty and Schneebeli, 1955; Kramer et al., 1957) . In 

 addition to their catabolic effect on protein, the carbohydrate-active corti- 

 coids have specific suppressive effects on osteogenesis, chondrogenesis, 

 mitosis, growth in general, connective tissue growth, inflammation, phago- 

 cytosis, granulation, and antibody formation (Taubenhaus and Amromin, 

 1950; Baker, 1950, Selye, 1951; Dorfman, 1953; Dougherty, 1953; Tauben- 



