CARBOHYDRATES. 81 



urine of frogs with extirpated livers, it is probable that the glucosuria is 

 to be attributed to a disturbance of the liver function. It might be sup- 

 posed that the sugar elimination in the urine is a result of the tetanus 

 produced by the strychnine poisoning. That this is not the case is shown 

 by the fact that animals poisoned with large amounts of strychnine large 

 doses, instead of producing tetanus, cause paralysis of the motor nerves 

 are also subject to glucosuria, and, as a matter of fact, in a more severe form 

 than in the case of animals with tetanus, caused by smaller doses of strych- 

 nine. The simplest explanation of this last fact is that during tetanus 

 sugar is consumed. Other poisons, such as phosphorus, arsenic, uranium 

 salts, corrosive sublimate, carbon monoxide (illuminating-gas), amyl 

 nitrite, curari, chloral, nitrobenzene, chloroform, acetone vapors, ether, 

 etc., will also cause glucosuria. 1 At present we know nothing more definite 

 concerning the mode of action of these various substances. It should not, 

 however, be assumed that they all have the same point of attack. 



The glucosuria produced by the glucoside phloridzin has been studied 

 with especial thoroughness. 2 If from one to three grams of this sub- 

 stance is administered to a dog for each kilogram of its body weight, 

 glucosuria results. In the case of starving animals, after the injection 

 of from 0.3 to 2.5 grams of phloridzin, the sugar can be found in the 

 urine. Von Mering, the discoverer of this form of glucosuria, also studied 

 the effect of the decomposition products of phloridzin, and found that 

 phloretin alone was active in this respect, whereas phloroglucinol and 

 phloretic acid were inactive. 



All the other glucosurias which we have discussed up to this point have 

 been caused by a glucohemia, i.e., a flooding of the organism and especially 

 of the blood with sugar. The elimination of sugar through the kidneys 

 is a result of a self-regulating mechanism. By eliminating the excess of 

 sugar the organism seeks to bring the sugar content of the blood back to 

 the normal. Even the glucosuria produced by phloridzin has been ex- 

 plained in this way, 3 although Mering himself and many other later inves- 

 tigators have failed to detect any increase in the amount of sugar contained 

 in the blood even when the ureter was tied. Phloridzin glucosuria is also 



1 Cf. Langendorff: Arch. Anat. Physiol. 138 (1887). F. Giirtler: Inaug. Dissert. 

 Konigsberg, 1886. Araki: Z. physiol. Chem. 17, 311 (1893). Luchsinger: Inaug. 

 Dissert. Zurich, 1875. Senff : Inaug. Dissert. Dorpat, 1869. Straub: Arch, exper. Path. 

 Pharm. 38, 139 (1897). Rosenstein: ibid. 40, 363 (1898). Araki: Z. physiol. Chem. 

 15, 351 (1891); 19, 422, 476 (1894); also Bernard: LeQons sur la diabete et la gly- 

 cosurie animale. Paris, 1877. 



2 v. Mering: Ueber Diabetes mellitus. Verhandl. Kongr. innere Med., 1886 u. 1887; 

 Z. klin. Med. 14, 405 (1888), and 16, 431 (1889). v. Mering and Minkowski: Zentr. klin. 

 Med. 10, 393 (1889). Max Cremer: Z. Biol. 29, 175 (1893). Cremer and Ritter: ibid. 

 29, 256 (1893). 



3 Cf. Pavy: J. Physiol. 20, xix-xxii (1896). S. Leone: Gazz. internaz. di med. prat. 

 Vol. 3, 21. 



