Antiketogenesis

In addition to these interconversions, the metabolism of fat and the metabolism of carbohydrate are inseparably related. This fact is most clearly demonstrated by the appearance of such abnormal products of fat oxidation as the so-called ketone bodies in the blood and urine whenever the supply of carbohydrate is deficient or in cases where the organism is unable to metabolize this foodstuff. Whether ketonuria results because the metabolism of fat must occur concomitantly with that of D-glucose (ketolysis), or whether the presence of D-glucose prevents any fat breakdown because it is preferentially oxidized (antiketogenesis) is still a moot question. 

On the other hand, there are a number of experiments which indicate that a relationship must exist between the oxidation of the ketone bodies and sugar these cannot be explained on the antiketogenesis theory. The strongest in vitro proof was originally demonstrated by Shaffer178 and has since been extended by West.179 180... 

Further evidence is afforded by the in vivo experiments where it has been shown that only D-glucose and D-glucose-precursors are able to lower ketonuria. According to the antiketogenesis theory, any readily metabolizable sources of calories should be able to suppress the oxidation of an isodynamic quantity of fat and so prevent the formation of the... 

The reaction of D-glucose with ethyl acetoacetate was originally studied with a view to obtaining experimental information which would be useful in the interpretation of the biological phenomena of antiketogenesis. It is accepted that some kind of correlation exists between the metabolism of carbohydrates and that of /3-ketonie compounds, but views as to its nature differ. The supporters of the ketolysis theory1 contend that the oxi-... 

These data on fasting ketonuria in man as well as the earlier described tests on the exogenous and endogenous ketonuria of rats indicate that marked changes in ketonuria can occur after the administration of carbohydrate in quantities too small to decrease significantly the fat catabolism. It is difficult to harmonize such results with the antiketogenesis theory. 

However, it has long been known that sorbitol is antiketogenic. If the reaction described above is the sole manner in which sorbitol is inserted into the metabolism, this would suggest that the dehydrogenation itself, leading to a depletion of oxidized DPN, is the source of the antiketogenesis. 

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