Studies on the effect of fructose and xylitol in the rat liver: 5'-nucleotidase, adenosine deaminase, de novo purine synthesis.

Abstract

Fructose as well as xylitol are both rapidly metabolized in liver the main product being glucose (1, 11). In high doses these sugar surrogates induce an increase of uric acid levels both on parenteral and oral application (4, 5, 8, 14, 16, 18, 20). The causes underlying the hyperuricemia thus produced are still unclear. Since the metabolism of both substrates involves a phosphorylation step, the liver cell ATP concentration is (at least temporarily) reduced. This reduction is accompanied by a depletion of ADP, AMP and inorganic phosphates. The loss of inorganic phosphates (Pi) is thought to activate catabolic enzyme reactions of purine metabolism which, in turn, would enhance purine nucleotide degradation (2, 5, 12, 17 – 20). If this hypothesis is correct, both fructose and xylitol should be expected to activate catabolic enzymes, such as 5′-nucleotidase and adenosine deaminase. This, in turn, would result in a secondary increase of de novo purine synthesis. To validate this assumption we studied the effects of the two sugar alcohols on 5′-nucleotidase and adenosine deaminase activities in the rat liver in vivo and in vitro. At the same time, the incorporation of the purine precursor glycine in rat liver adenine nucleotides was measured.