CLARA M. SZF.C.O 



155 



occurrence of this antagonistic relationship between estradiol and certain 

 structurally related compounds furnishes a valuable clue to the mechanism of 

 steroid hormone action and interaction, particularly since it has permitted a 

 certain degree of dissociation of the so-called primary from the secondary 

 phenomena (cf. 24, 36). 



INFLUENCE OF STEROIDS ON UTERINE RESPIRATION AND GLYCOLYSIS 



It may be anticipated that the metabolic transformations which accompany 

 growth in a hormonally stimulated sexual target structure would be associated 

 with enhancement in energy metabolism. In fact, respiratory and glycolytic 

 mechanisms in this organ have previously been shown to be stimulated about 

 24 hours after the subcutaneous administration of estrogenic hormone (6, 16). 

 In our studies (25), significant changes in the respiration of surviving uterine 

 tissue obtained from ovariectomized rats could be demonstrated within a few- 

 hours after the intravenous administration of 0.5 microgram of estradiol per 

 100 grams body weight (fig. 2). Actually, in the absence of added glucose in the 

 incubation medium {open circles), significant increases were noted in the tirst 

 hour after estrogen injection. The presence of glucose {solid circles) in almost 

 every instance depressed the respiration of surviving uterine tissue from estro- 

 gen-treated castrated rats and tended to mask these early evidences of stimu- 

 lation. The total oxidative metabolism of this tissue reached a maximum about 

 16-20 hours after estrogen administration. A second peak in water imbibition 

 also occurred during this period {uppermost curve). Both processes were pre- 

 sumably associated with the stimulation of true growth of the uterus which 

 occurs about this time. 



In the presence of added glucose, aerobic incubation of the uterus of the 

 untreated castrated rat resulted in the disappearance of large amounts of this 

 carbohydrate, as depicted by the open circle at zero time in figure 3. About 

 two-thirds of this could be accounted for by the accumulation of lactate {solid 

 circle) . 



The early electrolyte and water changes in the uterus, occurring a few hours 

 after the intravenous administration of estrogen, were accompanied by a strik- 

 ing enhancement in carbohydrate utilization by this organ. Much of the extra 

 glucose which disappeared at this time (4 hr.) was apparently converted to 

 lactate. Since the increase in uterine respiration in the glucose medium at this 

 time was of only limited significance (tig. 3, crosses), it must be assumed that 

 metabolic shifts occurred within the uterus as a result of estrogenic stimulation, 

 which facilitated the increased permeation and utilization of glucose and the 

 sparing of endogenous substrate. 



It will also be noted in figure 3 that a slight decrease in glucose utilization 

 occurred after the 4-hour peak. A renewed disappearance of carbohydrate 

 became evident during the secondar}^ growth phase and reached a maximum 



