DR. PAVY AND DIABETES 33 



is probable at least that they are determined by specific 

 enzymes. To some upset in the normal equilibrium of such 

 enzymic activity may be ascribed the fact that on rare occasions 

 fructose is excreted by individuals even when their diet contains 

 no carbohydrate which could yield fructose during digestion. 

 In such cases the normal direction of isomeric change would 

 appear to have suffered reversal, fructose being formed from 

 dextrose. For it is usually and very justifiably assumed that 

 normally, while dextrose is directly taken up by a cell, the 

 isomeric sugars are converted into dextrose before the metabolic 

 grip takes hold upon them. A certain speculation, however, 

 with regard to this matter may be excused. Yeasts can ferment 

 any of the above three sugars with approximately equal ease 

 and the fermentative breakdown in each case is on precisely 

 similar lines. It has been suggested that the reason for this 

 is that the fermentation starts with identical material in each 

 case— namely, the enol of the sugars produced by a preliminary 

 enzymic change. 1 If this suggestion have any weight in con- 

 nexion with fermentation, it is justifiable to apply it to the 

 animal cell ; and if dextrose itself must be enolised before the 

 cell can condense it to glycogen or impress other changes upon 

 it, it is clearly possible that the metabolic failures responsible 

 for glycosuria may include a failure to enolise. The conversion 

 of any one of these related sugars to the enol form may perhaps 

 be conditioned by a distinct enzyme, so the interesting but very 

 obscure circumstance that diabetics can often utilise fructose 

 when their power to utilise an equal quantity of dextrose is 

 lost lends some support to the above conception. It must be 

 admitted, however, that it is essentially speculative. 



We shall in any case clearly gain light upon the normal 

 metabolism of sugar if we can decide what precisely is absent 

 when, in conditions of clinical or experimental diabetes, the 

 body fails to oxidise that substance. The deficiency is by no 

 means the same in all varieties of diabetes or glycosuria and 

 the hope is reasonable that by the time we have classified these 

 varieties we shall know something of more than one of the 

 links in the chain of normal metabolic change. A fact of great 

 significance is that in spite of the failure to oxidise sugar, the 

 diabetic organism shows no failure in general oxidation power. 



1 Cf. E. F. Armstrong, The Simple Carbohydrates and the Glucosides 

 (Longmans, 1910), pp. 52 et seq. 



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