692 METABOLISM 



tion of the amount of ingested carbohydrate required to bring about post- 

 prandial glycosuria constitutes, as we have already seen, the so-called 

 assimilation limit for sugar, which is often taken as an index of the sugar- 

 metabolizing power of the organism. It is evident, however, that the time 

 of onset, and the extent and duration of postprandial hyperglycemia must 

 serve as a more certain index of the sugar-retaining power of the liver 

 and muscles; and now that several simple and rapid clinical methods 

 exist (Lewis-Benedict or Maclean methods) for the accurate determina- 

 tion of sugar in small quantities of blood, there is no reason why this 

 index should not be used for the detection of failing powers to metabolize 

 carbohydrate. 



In no disease, probably not even in tuberculosis, is it more important 

 than in diabetes that an early diagnosis should be made. Thus, if we find 

 that the postprandial hyperglycemia after a certain amount of carbo- 

 hydrate develops to an unusually high degree and persists for an unusual 

 length of time, we are justified in curtailing the carbohydrate supply so as 

 to hold these values down to the level they attain in normal individuals. 

 It is almost certain that the earliest sign of diabetes is an unusual degree 

 and duration of postprandial hyperglycemia. At first the excess of sugar 

 leads to no damage and it is insufficient to cause any evident glycosuria, al- 

 though it is quite likely that if the urine in such individuals were collected 

 at very frequent intervals after eating carbohydrate-rich food, glucose would 

 be found present in at least some of the specimens. In incipient diabetes, 

 however, the condition progresses, until the postprandial hyperglycemia 

 after one meal has not become entirely replaced before the next is taken, 

 so that the increase in sugar produced by the second meal becomes super- 

 added on that following the first meal. The curve of blood sugar rises 

 ever higher and higher, until at last permanent hyperglycemia is estab- 

 lished, or rather the normal level from which the postprandial rise occurs 

 has become permanently raised, so that in blood collected at any time a 

 higher percentage of sugar is found. 



The Relationship Between the Sugar Concentration of the Blood and 

 the Occurrence of Glycosuria. Claude Bernard first pointed out that the 

 percentage of sugar in the blood may rise considerably above its normal 

 level without the appearance of any of the sugar in the urine, or at least 

 without a sufficient amount to give the usual tests for sugar. Even when 

 this limit is reached, as we have seen, the sugar which appears is not all of 

 the excess but only a small part of it. This overflow hypothesis, as it is 

 called, has not been universally accepted because of the many results 

 which are not in conformity with it. Many of these exceptional results 

 have been explained as due to alterations in the permeability of the kidney 

 for sugar, and in general it is probably safe to accept Claude Bernard's 

 hypothesis with certain reservations. 



