Aldolase B !

Liver aldolase B splits fructose 1-phosphate into two trioses; if it is missing, dietary fructose becomes toxic.

Updated 2026-11-01

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Key facts

Fructose 1-phosphate → DHAP + glyceraldehyde; it also splits fructose 1,6-bisphosphate (glycolysis and gluconeogenesis).
Isoenzymes: A (muscle and red cell), B (liver, kidney, intestine) and C (brain); only B handles fructose 1-phosphate well.
It uses an active-site lysine that forms a Schiff base with the substrate (class I aldolase).
Structure 1QO5 (human liver) has only sulfate ions in the active site, where the substrate phosphates sit.

It is induced by a diet rich in carbohydrate and fructose; insulin increases its liver expression.

Its deficiency is hereditary fructose intolerance: hypoglycaemia, vomiting and liver and kidney damage after fructose, sucrose or sorbitol.
The most common variant in people of European descent is A149P.

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Which substrate sets aldolase B apart from aldolase A?

Fructose 1-phosphate: B splits it well; A hardly at all.

Why does aldolase B deficiency cause hypoglycaemia?

Accumulated fructose 1-phosphate traps phosphate and blocks glycogen phosphorylase and gluconeogenesis.

In which organs is aldolase B expressed?

Liver, renal cortex and small intestine.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: ALDOB: Fructose-bisphosphate aldolase B (human) (UniProt, 2026); ALDOB gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); 1QO5: Fructose 1,6-bisphosphate Aldolase from Human Liver Tissue (RCSB Protein Data Bank, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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Representative model, for educational purposes only.