66 Cramer and M'Call 



where, as in tlie case of Rat 3, the quotient never rises even as high 

 as 0-85. 



Such abnormally low (|Uotients, obtained after a meal rich in carbo- 

 hydrates, cannot be explained in this case as being due to an impaired 

 oxidation of carbohydrates. We know that thyroid feeding prevents the 

 storage of carbohydrates in the liver. If in addition to the inability to 

 store carboh3^drates there were also an impaired oxidation of carbo- 

 hydrates, experimental hyperthyroidism ought to produce a severe 

 diabetes mellitus. But, as has been mentioned in the Introduction, and 

 as we have repeatedly tested in the course of these experiments, it does 

 not even produce a glycosuria. Another reason for excluding an impaired 

 oxidation of carbohydrates as a possible explanation is that it would be 

 almost impossible to understand how thyroid feeding could, under 

 apparently identical experimental conditions, produce two diametrically 

 opposed conditions, even in the same animal (Rat 1 at different times). 



One must therefore look for a different explanation of the lowering 

 of the quotient when it occurs. The only other known cause which 

 could account for it under the conditions of our experiments is the 

 transformation of protein and possibly fat into carbohydrate. These 

 processes lower the quotient by increasing the absorption of Og. The 

 carbohydrate thus formed from protein and fat is not deposited, but at 

 once oxidised. 



The increased breakdown of protein and disappearance of fat which 

 this explanation presupposes is a well-known and long-established effect 

 of thyroid-feeding. It appears on our interpretation as a secondary 

 result of the action of the thyroid secretion on the glycogenic function 

 of the liver. The more protein or fat is transformed into carbohydrate 

 and then oxidised, the more the curve of the respiratory quotient will 

 be depressed. A low-level curve thus indicates that a relatively large 

 amount of protein or fat is being transformed into carbohydrate and 

 oxidised as such, while a high-level curve signiiies that the carbohydrate 

 which is being oxidised is mainly that pre-existing in the food or still 

 present in the organism. 



The correctness of the explanation which has been given can be tested 

 by the observations recorded in this paper. The greater the amou)it of 

 protein or fat transformed into carbohydrate, the greater will be the amount 

 of carbohydrate undergoing oxidation. The measure of the first-mentioned 

 process is the level of the respiratory quotient curve : the lower the level 

 the greater the amount of protein or fat undergoing transformation. The 

 measure of the second process is the increase in the COo excretion above 

 that of the normal animal. One should therefore expect to find that the 

 lower the level of the respiratory quotient curve the higher the level of 

 the CO2 excretion. A glance at the figures shows that this is the case. 

 In Rat 1, second series, and Rat 8, where the respiratory quotient curve 

 is very low, the increase in the COg excretion is much greater than in 



