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Vitamin B5: the pathway in the body

This page shows the biochemical pathway behind the laboratory value Vitamin B5 (pantothenic acid): which stations follow one another, which enzymes carry out each step and which cofactors they use. Every statement has a source. The page describes general textbook knowledge and says nothing about any individual person.

In brief

Vitamin B5 (pantothenic acid) is a water-soluble vitamin found in almost all foods. The cell uses it to build coenzyme A, which activates fragments from sugar, fat and protein and so links energy production, fatty-acid metabolism and many building pathways.

12 stations · 5 sources
ORYAbsorptionAction in the cellPANK, PPCS, PPCDCATPcysteinePDH complexcoenzyme Aacyl-CoA synthetasecoenzyme AATPpantetheinaseSMVTsodiumCOASYATPcarnitinevia SMVT into the cellPantothenic acid (food)mostly bound as coenzyme AFree pantothenic acidin the small intestinePantothenate in blooddissolved freelyPantothenic acid (cell)absorbed via SMVT4'-PhosphopantetheineintermediateCoenzyme ACoA, active formPyruvatefrom glucose breakdownAcetyl-CoAactivated acetic acidFatty acidfrom food or fat storesAcyl-CoAactivated fatty acidCitric acid cycleenergy metabolismβ-Oxidationin the mitochondrion

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The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

  1. Pantothenic acid (food) → Free pantothenic acid pantetheinase Phosphatases in the gut break coenzyme A down step by step to pantetheine; the enzyme pantetheinase splits free pantothenic acid from it. Only this form is absorbed. Source 1↑ supplies Only as the free acid does the transporter SMVT recognise the vitamin; the same transporter also absorbs biotin and lipoic acid. established physiology Source 1
    ⚖ When the balance tips

    too much — If a lot of free pantothenic acid is present, it competes with biotin for the same transporter.

    too little — If little is released, less pantothenic acid is available for the transporter to absorb.

    established physiology · Source 1

  2. Free pantothenic acid → Pantothenate in blood SMVT · sodium The transporter SMVT carries pantothenic acid together with sodium into the gut cell; from there it reaches the blood. The kidneys excrete any excess. Source 1↑ supplies The blood distributes pantothenic acid to all tissues; every cell makes its own coenzyme A from it. established physiology Source 1, 2
    ⚖ When the balance tips

    too much — If pantothenic acid in the blood rises, the kidneys excrete the excess in the urine.

    too little — If little follows from the gut, the supply to the tissues falls and cells make less new coenzyme A.

    established physiology · Source 1

  3. Pantothenic acid (cell) → 4'-Phosphopantetheine PANK, PPCS, PPCDC · ATP, cysteine Pantothenate kinase (PANK) attaches a phosphate, then cysteine is added and loses a carbon dioxide. This produces 4'-phosphopantetheine with its sulphur group. Source 2, 3↑ supplies 4'-Phosphopantetheine carries the sulphur group to which acyl residues are later bound; it also sits as a fixed arm in fatty acid synthase. established physiology Source 2, 3
    ⚖ When the balance tips

    too much — If a lot of it is present, it is built on to coenzyme A, and feedback on PANK limits further supply.

    too little — If the PANK step is slow, little 4'-phosphopantetheine forms, and both users, coenzyme A and fatty acid synthase, receive less.

    established physiology · Source 3

  4. 4'-Phosphopantetheine → Coenzyme A COASY · ATP The enzyme COASY attaches part of an ATP in two steps; coenzyme A is then complete. Its sulphur group binds acyl residues such as the acetyl group. Source 2, 3↑ supplies Coenzyme A activates fragments from sugar, fat and protein by binding them to its sulphur group in an energy-rich bond; enzymes can then transfer, break down or assemble them into new molecules. established physiology Source 2, 3
    ⚖ When the balance tips

    too much — If a lot of coenzyme A is bound as acyl-CoA, it slows its own formation at PANK and inhibits individual metabolic enzymes.

    too little — If little free coenzyme A is available, pyruvate dehydrogenase, the citric acid cycle and fatty-acid breakdown stall, because they need it for every turnover.

    established physiology · Source 2, 3

  5. Pyruvate → Acetyl-CoA PDH complex · coenzyme A Pyruvate dehydrogenase removes carbon dioxide and attaches the rest to coenzyme A. Acetyl-CoA is the central hub of metabolism. Source 4, 2↑ supplies Acetyl-CoA feeds the citric acid cycle and is a building block for fatty acids, cholesterol, steroid hormones and the messenger acetylcholine; as an acetyl group it also modifies proteins. established physiology Source 2
    ⚖ When the balance tips

    too much — If acetyl-CoA builds up, it slows pyruvate dehydrogenase, and the liver forms more ketone bodies.

    too little — If little acetyl-CoA forms, the citric acid cycle receives less fuel and less building material is available for fatty acids and cholesterol.

    established physiology · Source 2, 4

  6. Fatty acid → Acyl-CoA acyl-CoA synthetase · coenzyme A, ATP Acyl-CoA synthetase joins the fatty acid to coenzyme A, using ATP. Only in this form can the cell break it down or build it into fats. Source 5, 2↑ supplies Acyl-CoA is the form in which fatty acids reach the mitochondrion via the carnitine route or are built into fats and membrane components. established physiology Source 5
    ⚖ When the balance tips

    too much — If acyl-CoA builds up, it ties up a large share of coenzyme A; the cell copes by passing acyl groups to carnitine.

    too little — If little free coenzyme A is available, fewer fatty acids are activated and less enters breakdown.

    established physiology · Source 2, 5

  7. Acetyl-CoA → Citric acid cycle In the citric acid cycle the acetyl group is broken down completely to carbon dioxide; coenzyme A is released and is available again. Source 2↑ supplies The citric acid cycle supplies electrons for the respiratory chain, where ATP is made; with succinyl-CoA it needs coenzyme A once more itself. established physiology Source 2
    ⚖ When the balance tips

    too much — If a lot of acetyl-CoA arrives, the cycle runs as fast as NAD⁺ and oxygen allow; the rest goes into fatty acids or ketone bodies.

    too little — If little acetyl-CoA arrives, fewer electrons are produced for the respiratory chain.

    established physiology · Source 2

  8. Acyl-CoA → β-Oxidation · carnitine With the help of carnitine the activated fatty acid reaches the mitochondrion. There it is broken down in two-carbon pieces, each released as acetyl-CoA. Source 5↑ supplies Each round of β-oxidation needs fresh coenzyme A and yields acetyl-CoA as well as electrons to FAD and NAD⁺. established physiology Source 5
    ⚖ When the balance tips

    too much — If a lot of β-oxidation runs, more acetyl-CoA forms than the citric acid cycle can absorb; the liver turns it into ketone bodies.

    too little — If little carnitine or coenzyme A is available, fewer fatty acids enter breakdown and they tend to be stored as fat.

    established physiology · Source 5

Further stations

Cofactors in this pathway

Sources

  1. Said HM, Nexo E. Gastrointestinal Handling of Water-Soluble Vitamins. Compr Physiol 2018 · PubMed 30215865
  2. Czumaj A, Szrok-Jurga S, Hebanowska A et al. The Pathophysiological Role of CoA. Int J Mol Sci 2020 · PubMed 33260564
  3. Srinivasan B, Sibon OC. Coenzyme A, more than 'just' a metabolic cofactor. Biochem Soc Trans 2014 · PubMed 25110005
  4. Patel MS, Nemeria NS, Furey W et al. The pyruvate dehydrogenase complexes: structure-based function and regulation. J Biol Chem 2014 · PubMed 24798336
  5. Longo N, Frigeni M, Pasquali M. Carnitine transport and fatty acid oxidation. Biochim Biophys Acta 2016 · PubMed 26828774

Related pathways

As of 2026-10-05. Draft written by Claude to schema v2; sources checked in PubMed; expert review pending
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