Abstract
Ribose synthesis in vivo was studied by isolating imidazoleacetic acid riboside from rats given imidazoleacetic acid and a C14-labeled sugar. Evidence is presented which indicates an impairment of riboside excretion in partially hepatectomized and in diabetic animals. The isotope distribution in ribose synthesized from glucose-2-Cl4 by normal animals is consistent with synthesis via both the oxidative and the nonoxidative reactions of the pentose phosphate pathway. Thiamine deficiency resulted in a marked decrease of ribose synthesis from hexose via the nonoxidative mechanism. An apparent increase in ribose production by way of the oxidative reactions was observed in rats with regenerating livers and in tumor-bearing animals. These observations are discussed in the light of our present concepts of the role of the oxidative reactions in reduced triphosphophyridine nucleotide (TPNH) production for synthetic processes. Evidence is presented for the direct incorporation of administered ribose into urinary riboside.