Phosphoenolpyruvate carboxykinase (PEPCK) !

PEPCK turns oxaloacetate into phosphoenolpyruvate using GTP; it is a key gluconeogenic enzyme switched on by glucagon and off by insulin.

Updated 2026-11-01

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Key facts

Oxaloacetate + GTP → phosphoenolpyruvate + GDP + CO₂.
Together with pyruvate carboxylase it goes around the irreversible pyruvate kinase step; the pair costs 2 high-energy bonds per pyruvate.
It is regulated by the amount of enzyme (transcription), not allosterically: glucagon (cAMP) and cortisol induce it; insulin represses it.
There is a cytosolic form (PCK1, the main one in the liver) and a mitochondrial form (PCK2).

In adipose tissue PEPCK serves glyceroneogenesis: it forms glycerol 3-phosphate to re-esterify fatty acids.
Excess glucocorticoids (Cushing syndrome or long-term therapy) increase PEPCK and blood glucose.
Cytosolic PEPCK deficiency is very rare and causes fasting hypoglycaemia.

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Which nucleotide does PEPCK use as its phosphate source?

GTP; that is why gluconeogenesis spends 2 GTP per glucose.

How does insulin regulate PEPCK?

It represses PCK1 gene transcription and lowers the amount of enzyme.

Why does excess cortisol raise blood glucose?

Among other effects it induces PEPCK and glucose-6-phosphatase and increases hepatic gluconeogenesis.

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

Sources: PCK1: Phosphoenolpyruvate carboxykinase, cytosolic [GTP] (human) (UniProt, 2026); 1KHF: PEPCK complex with PEP (RCSB Protein Data Bank, 2026); Gluconeogenesis (Reactome, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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