I III Mi i UBOLIS M OP i III I ARBOHYDB \ I 



its pancreas, it will restore it to a nondiabetic stale. The al con- 



clusion thai may be drawn from the numerous researches of this nature 

 is thai tlinc is no evidence thai the blood of a normal animal, e 

 when it is from the pancreatic vein, contains an internal secretion that 

 can restore to a diabetic animal any of its losl power to utilize carbo- 

 hydrates. When the extent of glycosuria alone is used as the criterion 

 iif the state of carbohydrate metabolism, serious errors in judgmenl are 



liable t<> be drawn. The condition of the blood mcmt ami the extent 



ami character of the respiratory exchange arc the mosl reliable [nde: 



DIABETIC ACIDOSIS OR KETOSIS 



Nature and Cause. Much confusion lias existed in medical literature 

 over the correcl definition of acidosis, mainly because the term was firsl 

 used for the particular variety of the condition observed in th< 

 stages of diabetes mellitus. The acids which accumulate in the ti- 

 fluids in this disease arc acetoacetic ami /8-oxybutyric, which are re- 

 lated to acetone ami are derived from fatty acids by a faulty metabo- 

 lism i see pane 709). The essential cause of the acidosis is therefore 

 entirely different from that in nephritis; in diabetes foreign acids are 

 added to the blood, whereas iii nephritis the acids of a normal metabo- 

 lism accumulate because of faulty excretion through the kidneys. The 

 usual siL r ns nt' acidosis exist in both cases, because the surplus of acid 



depletes ihc store of 1 >ica rl 1011a I e and causes changes in the al- 

 ar < <> . in the C0 2 -absorbing power of the blood, in the reserve al- 

 kalinity, and in the acid excretion by the kidney. It is important t.> 

 recognize the special nature of diabetic acidosis by a separate name — 

 l,i tosis. 



The chemical processes by which the ketone bodies are produced is 

 discussed elsewhere (page T « ^ * . It remains for us to consider the 

 general nature of the metabolic disturbance responsible for their ap- 

 pearance in diabetes. 



For the thorough combustion of fat in the animal body a certain 

 amounl of carbohydrate must be simultaneously burned. Fat evidently 

 is a hss readily oxidized foodstuff than sugar; it needs the tire of the 

 burning sugar to consume it. If the carbohydrate fires do not burn 

 briskly enough, the fal is incompletely consumed; it smo 

 and the smoke is represented in metabolism by the ketones and der 

 acids. Such a closing <lown of the carbohydrate furnaces may 

 brought aboul either by curtailment of the intake of carbohydral 

 in starvation (page 569), >t bj Home fault in the mechanism of the 

 furnace itself, as in diabetes Besides fat, protein may als tribute 



