rillA)l{IIIZI\ DIMiETES 659 



Certain (itlicr (lrii<is, siu-h as ciu-an', strycliiiiu, etc., may iiitcrfei'c 

 with res{)irat()rv moveiiieiits and so cause glycosuria by secondary 

 asphyxia; althougli other drugs, of which tliere are many, may op- 

 erate to cause glycosui-ia in any of the waj's by which glycosuria can 

 be produced. ■''*' 



(c) The ductless gland extracts which produce glycosuria include 

 those of the adrenal, thyroid and hypophysis. Epinephrine has been 

 discussed in another place, and the reasons are there developed for the 

 belief that the glycosuria it causes is due to a mobilization of sugar 

 from glycogen, which leads to hyperglycemia. Kinger ^' showed that 

 when an animal is fully ])hlorhizinized the svd)cutaneous injection of 

 epinephrine causes no additional output of sugai' nor alteration of the 

 G : N ratio, a fact which has been contirmed by Sansum and AA^'oodyatt 

 — thus proving that epinephrine has no power to intensify a diabetes 

 which is already at the point which is called complete. Lusk ^** also 

 showed by respiration experiments the correctness of this interpreta- 

 tion. Eppinger, Falta and Rudinger ^^ stated that epinephrine inten- 

 sifies pancreas diabetes, and used this observation in support of their 

 idea that epinephrine, like thyroid extract, exerts in the liver a sugar- 

 mobilizing and sugar-building etfect, antagonistic to the action of the 

 pancreas, which, according to the doctrine of the von Noorden school, 

 cheeks the formation of sugar from glycogen and also from protein 

 and fat. But in their work there has been no adequate proof that be- 

 fore giving the epinephrine the pancreas diabetes was as complete as a 

 pancreas diabetes can be, or that the increased intensity of the dia- 

 betes was any greater than could have been explained by a discharge 

 of sugar from glycogen. The power of pituitary extracts to produce 

 glycosuria is likewise aseribable to their effects on glycogen. 



PHLORHIZIN DIABETES^" 



Phlorhizin was obtained by alcoholic extraction of the bark and 

 roots of apple, pear, plum and cherry trees by L. de Koninck in 

 1835. Its glucosidic character was established by Stas, who found 

 that it could be split into glucose ("phlorose") and a substance 

 (phloretin) which by acid hydrolysis yielded i)hloroglucin and an 

 acid (phloretinic acid). It was not until 1886 that von Mering 

 published his first experiments upon its physiologic action. 



30 The production of <jlycosiiria by a piven clni<r should not be confused with 

 an excretion of yiaired <rlycuronic acid compoiuids. sucli as occurs after the 

 administration of many aldehydes, ketones, alcohols and phenols. The re- 

 ducino- power in these cases is not due to glucose but to its oxidation product, 

 COOH— ( CHOII ) ,— -COH. 



37 Jour. Kxper. INIed., 1010 (12), 105. 



3s Arch. Int. Med., 1014 (13). 67.3. 



30 Zeit. f. klin. Med., lOOS (fifi). 1: 1900 (671, 3R0. 



4" For a treatise of the wliole subject of phlorliizin glycosuria, with bibliography, 

 see the monograph by Lusk (Phlorhizin Glykosurio, Ergeb. der Physiol., 1012 

 ( 13 ) , 315 ) , free use of which has been made in the following. 



