60 Cramer and JM'Call 



stimulates the oxidation of carbohydrates, has ah-eady been considered by 

 Cramer and Krause and was excluded by them on the ground that 

 glj'cogen is absent from the liver even immediately after a meal rich in 

 carbohydrates, whereas one would expect to find only a more rapid dis- 

 appearance of glycogen from the liver of thyroid-fed animals and a 

 replenishing after a meal if the effect on the liver glycogen were merely a 

 secondary one. The conclusion that this possibility must be excluded is 

 confirmed by other facts. If the thyroid hormone produced a direct 

 stimulating effect on the oxidation of carbohydrates, one would expect that 

 hj^perfunction of the thj'roid gland, whether produced experimentally by 

 thyroid-feeding or studied clinically in Graves' disease, should produce a 

 rise in the limit of assimilation for sugar. It is well known that in Graves' 

 disease this is not the case ; on the contrary, there is frequently a tendency 

 to glycosuria in that condition. The effects of thyroid-feeding which have 

 been studied in dogs show a slight but distinct lowering of the limit of 

 assimilation for glucose. Conversely, one would expect that thyroid 

 insufficiency, whether studied clinically in myxcfdema or produced 

 experimentally by extirpation of the gland, should lead to an impaired 

 oxidation of carbohydrates and therefore a lowering of the limit of 

 assimilation for glucose, if not actually a diabetes mellitus. Here again it 

 is well known in the case of mj^xredema that this is not the case, but that 

 there is a tendency in the reverse direction. The condition of the carbo- 

 hydrate metabolism in thyroidectomised animals, of which little is known, 

 has been studied by us in rats and may be dealt with in a subsequent 

 paper. It is sufficient to state here that our observations on the respiratory 

 quotient in thyroidectomised animals give no evidence of an impaired 

 power of oxidation of carbohydrates in thyroidectomised animals. This 

 is in agreement with the fact that thyroidectomy has never been found to 

 produce a diabetes mellitus, and that clinically diabetes has sometimes been 

 found to develop in persons suffering from Graves' disease, but not in 

 myx(vdematous patients (4). 



Moreover, if the thyroid secretion increased or facilitated the oxidation 

 of carbohydrates the thyroid hormone should represent the long-sought-for 

 remedy against diabetes mellitus. The literature contains no information 

 on this point. Our own experience is limited to one case of diabetes 

 mellitus, in which the condition was greatly aggravated by the administra- 

 tion of thyroid gland. 



The condition of the carbohydrate metabolism in a state of experimental 

 hyperthyroidism as induced by thyroid-feeding is therefore one which 

 cannot be accounted for by the orthodox conception of carbohj^drate meta- 

 bolism. We must therefore, in looking for an explanation, dispense with 

 the guidance offered by that theory and try to approach the problem 

 without the bias of a theory. 



Since in a state of experimental hyperthyroidism carbohydrates are 

 neither deposited as such nor excreted as such, nor transfoi-med into fats, 



