Fructose is a ketogenic monosaccharide that is broken down to form components for gluconeogenesis or glycolysis.
Fructokinase is an enzyme that causes the reaction of fructose into fructose-1-phosphate. Lack of fructokinase leads to developing the benign condition essential fructosuria.
Fructose is metabolized by fructokinase into fructose-1-phosphate (F1P). F1P is degraded by aldolase B into dihydroxyacetone phosphate (DHAP) as well as glyceraldehyde. Deficiency of aldolase B causes the condition fructose intolerance due to phosphate trapping due to increased amounts of fructose-1-phosphate.
There are three forms of the enzyme aldolase; aldolase A is expressed in muscle and brain, aldolase B in the liver and kidney, with and aldolase C in brain. Those with a deficiency of aldolase B have a disorder called hereditary fructose intolerance. In fructose metabolism, aldolase B facilitates the conversion of fructose-1-phosphate into dihydroxyacetone phosphate (DHAP) and glyceraldehyde. Within glycolysis, comparatively, aldolase converts fructose-1,6-bisphosphate into glyceraldehyde-3-P (G3P) and dihydroxyacetone phosphate (DHAP).
Fructose-1-phosphate is degraded by aldolase B into dihydroxyacetone phosphate (DHAP) and glyceraldehyde. A deficiency of aldolase B results in the accumulation of fructose-1-phosphate in cells.
Aldolase B catalyzes the formation of glyceraldehyde and DHAP.
DHAP and glyceraldehyde can both be converted into glyceraldehyde-3-phosphate, or G3P. G3P then enters the glycolysis pathway. Dihydroxyacetone phosphate (DHAP) is converted to G3P by triose phosphate isomerase and glyceraldehyde by triose kinase.