unreviewed

Citrate synthase

2 reactions · 2 pathways

Cofactors used

CoA-SH · B5 (Pantothenic acid) ATP H2O

Clinical / pharmacological. Entry step of TCA; inhibited by citrate, ATP, NADH, succinyl-CoA

What it does, reaction by reaction

2 reactions

Fatty Acid Synthesis (De Novo Lipogenesis) Lipid Metabolism · Cytosol

step 1 Irreversible/directional

Acetyl-CoA + oxaloacetate → citrate

Converts Acetyl-CoA Oxaloacetate into Citrate

› Notes

Mitochondrial citrate synthase condenses acetyl-CoA with oxaloacetate; it requires no ATP directly and releases CoA-SH. When energy is abundant, citrate accumulates and is exported through the tricarboxylate carrier. This is the initiating reaction of the citrate shuttle, not the committed step of fatty-acid synthesis.

Citric Acid Cycle (TCA / Krebs Cycle) Energy Metabolism & Cellular Respiration · Mitochondrial matrix

step 1 Irreversible

Oxaloacetate + acetyl-CoA + H2O → citrate + CoA-SH

Converts Oxaloacetate Acetyl-CoA H2O into Citrate CoA-SH

› Notes

Cofactors: no redox cofactor; water hydrolyzes the thioester, and CoA-SH is released. This strongly exergonic, essentially irreversible step is a major control point and commits acetyl-CoA to citrate formation when oxaloacetate is available.

Showing all 2 reactions.

What accelerates and inhibits it

Regulation is pathway-specific, so each context is listed separately

1 entries

Citric Acid Cycle (TCA / Krebs Cycle)

Accelerated by

ADP; substrate availability (oxaloacetate and acetyl-CoA)

Inhibited by

ATP, NADH, citrate, succinyl-CoA

Hormonal control

No dominant acute direct hormonal switch; insulin increases carbohydrate-derived acetyl-CoA supply, whereas fasting/glucagon favor reduced TCA flux in liver when oxaloacetate is diverted to gluconeogenesis

Recent literature

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