Carl)ohy<lrate .Metabolism in relation to the Thyroid <ilat)d G7 



lull 1, Hrst series, or Kat 4, wlure the level ol" the respiratory quotient 

 curve is hij^h. Another suy^^restive fact is tliat un(l»'r tlie conditions of 

 these experiments tlie later stages of experimental hyjjertliyroidism appeared 

 on the third day, with the exception of Hat 2; and under the same con- 

 ditions it is on the second nr third (lay that the glyco;^en has completely 

 disiippeared fnjin the liver. 



Wlien thvroid feedin<r is discontiniKcl the miseous metabolism raTti<llv 

 retvn-ns to the normal. 



In the interpretation of the low (juotients given above it has not been 

 overlooked that a process involving the transformation of, say, protein 

 into carbohydrates and the subse(|uent oxidation of the carbohydrate 

 thus formed would, if considered in toto, give the same respiratory 

 quotient as the direct oxidation of the same amount of protein. One 

 might therefore be inclined to ask whether the interpretation which has 

 • been given is not merely a complicated way of exjnx'ssing the fact that 

 thyroid feeding produces an increased oxidation of carbohydrates, protein 

 and fat, and whether it would not be a simpler and e(|ually adccpiate 

 explanation of the phenomenon to assume that the thyroid hormone 

 increases all the oxidative processes of the cell ^ 



It is important to realise that such an explanation ditlers toto coelo 

 from the one given in this paper, in which the various changes in meta- 

 bolism are looked upon as secondary etiects which can be traced back to 

 the primary fact of the inhibition of the [glycogenic function of the liver. 

 The alternative explanation of an increased oxidative p(jwer of the cell 

 due to the thyroid hormone — a statement which in reality is not so much 

 an explanation as a paraphrase — interprets these changes as direct primary 

 effects. If an increased power of oxidation on the part of the cell were 

 the cause, the curve of the respiratory quotient of a thyroid-fed animal 

 should be essentially similar to that of a normal animal, while the curves 

 for the CO2 excretion and O^ absorption should run parallel to those of 

 the normal animal, but on a higher level. Moreover, it has already been 

 shown in this paper that the increased oxidation of carbohydrates cannot 

 be ascribed to a primary effect. We would therefore have to look upon 

 the increased oxidation of fat and protein as a separate and entirely 

 unrelated effect, which is superimposed upon the effect of the autacoid 

 of the thyroid gland on the liver glycogen and tlie resultant increased 

 oxidation of carbohydrates. Even then we should be unable to account for 

 the changes which the curves of the respiratory quotient and of the Oj 

 absorption undergo in the later stages of experimental hyperthyroidism. 



There are, moreover, several facts which point to the breakdown of 

 protein being secondary to the effect on the carbohydrate metabolism in 

 experimentaf hyperthyroidism. The first is that the transformation of 

 protein into carbohydrate occurs also in another condition associated with 

 the disappearance of glycogen from the liver, namely, in severe diabetes 

 mellitus. The difference is that in the latter condition the carbohydrate 



