Fructose is initially phosphorylated by liver fructokinase. Fructose is taken in by humans as sucrose, sucrose-containing syrups, and the free sugar. Fructose is mainly phos-phorylated to fructose-1-phosphate by liver fructokinase. Aldol cleavage by fructose-1-phosphate-specific aldolase, not enolase, yields glyceraldehyde and dihydroxyacetone phosphate. The glyceraldehyde is phosphorylated to glyceraldehyde-3-phosphate by triose kinase, and both triose phosphates can enter glycolysis. Excess fructose from commercial foods can exercise adverse effects by raising blood lipids and uric acid. Fructose phosphorylation bypasses phosphofructokinase, a regulatory enzyme of glycolysis and provides excess glycerol metabolites and excess triglyceride lipid biosynthesis. Fructose phosphorylation can also deplete liver cell ATP, lessening its inhibition of adenine nucleotide degradation and increasing production of uric acid. In adipocytes, fructose can be alternatively phosphorylated by hexokinase to fructose-6-phosphate. However, this reaction is competitively inhibited by appreciable amounts of glucose, as it is in other tissues.