INTERNAL SECRETION AND DISORDERS OF LIVER 675 



eventually by glycosuria. He also found that reflex excitation of the 

 bulbar center sufficed to produce the same phenomena. 



The importance originally attributed to the diabetes puncture, as dis- 

 covered by Bernard, gradually diminished as the result of later experi- 

 ments. Now it is generally accepted that there is no diabetogenic center 

 and that abnormal excitation of any important part of the nervous system 

 may directly or indirectly provoke glycosuria. 



Glycogen, which arises principally from the carbohydrates of foods, 

 functions as a reserve material analogous to vegetable starch, which plants 

 use as a source of energy. That, the glycogen content of the liver depends 

 essentially on the diet, has been clearly demonstrated by the fact that 

 during an absolute fast it almost entirely disappears from the liver (see 

 Pfliiger (a,) (&), 1903-05). 



The liver is not the sole organ concerned in glycogen formation. Ber- 

 nard (g) (1859), Nasse (1869) and many others have demonstrated glyco- 

 gen in the muscles. Kiilz (1890) found that the muscles also are capable 

 of fixing sugar and converting it into glycogen. Macleod and Funk (1917) 

 compared the sugar retaining ability of the liver and muscles during the 

 injection of moderate amounts of dextrose into the portal vein and found 

 that the sugar retaining power of the voluntary muscles is approximately 

 equal to that of the liver. Their experiments are opposed to the generally 

 accepted opinion 1 that the liver removes from the portal blood all the excess 

 of sugar added to it by intestinal absorption. Furthermore, Vezar (1911) 

 and others agree that the liver may not be necessary for the burning of 

 carbohydrate. This view is also confirmed by Eck fistula experiments. 



The constant presence of glycogen in the liver of dogs, fed for a long 

 time on an exclusive meat diet, indicated to Bernard that part of the 

 hepatic glycogen came from the alimentary proteins. Roily (1905), 

 Pfliiger (1907), Pfliiger and Junkersdorf (1910) and many others, by 

 starvation experiments on animals, have shown that the liver continues to 

 form glycogen, probably at the expense of the body protein, by cleavage of 

 the protein molecule. Pollak (1909) demonstrated that fasting rabbits, 

 and also those made glycogen-free by the administration of strychnin, can 

 by small increasing doses of epinephrin be made to store liver-glycogen in 

 a quantity only equaled in carbohydrate fed animals. But the muscles 

 remain entirely or almost devoid of glycogen. Reilly, Nolan and Lusk 

 (1898) showed that dogs with severe -phlorhizin diabetes continued to 

 excrete sugar, even when fed on protein alone or when starved. They 

 obtained a definite dextrose nitrogen ratio in the urine D : N : : 3.75 : 1, 

 which would indicate a sugar production from protein of nearly 60 per 

 cent. Dakin (1913) furnished direct evidence that some of the amino- 

 acids yielded by proteins may serve as a starting point for the formation 

 of glycogen. 



Glycogen may also arise from the decomposition of the fat molecule. 



