Vitamin B5 (Pantothensäure): the pathway in the body
Vitamin B5 (Pantothensäure) is part of the pathway “Vitamin B5”. This page shows the whole pathway; the station of Vitamin B5 (Pantothensäure) is highlighted.
Where this laboratory value sits: Pantothenate in blood — dissolved freely. 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
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 sourcesSwipe the graphic sideways
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.
- 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
- 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
- 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'-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
- 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
- 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
- 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
- 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
- Pantothenic acid (food) — mostly bound as coenzyme A
Pantothenic acid, vitamin B5, is found in almost all foods, for example offal, eggs, wholegrains and pulses. There it is mostly present as coenzyme A or its building blocks. Source 1, 2↑ supplies The body does not make pantothenic acid itself; what it needs for coenzyme A comes from food and in small amounts from gut bacteria.
established physiology Source 1
⚖ When the balance tips
too much — If a lot of pantothenic acid arrives, the transporter in the gut wall is soon saturated; a small part then enters by passive diffusion.
too little — If little arrives, supply depends more on the small store in the body and on what gut bacteria provide.
established physiology · Source 1
- Pantothenic acid (cell) — absorbed via SMVT
Cells bring in pantothenic acid via SMVT. In five steps they build coenzyme A from it. Source 2, 1↑ supplies Pantothenic acid is the part of coenzyme A that the body cannot make itself; the other building blocks come from cysteine and ATP.
established physiology Source 2
⚖ When the balance tips
too much — If a lot of pantothenic acid enters the cell, coenzyme A does not rise without limit: pantothenate kinase is slowed by coenzyme A and acetyl-CoA.
too little — If little pantothenic acid enters the cell, less coenzyme A is rebuilt as the existing pool is broken down.
established physiology · Source 2, 3
- Pyruvate — from glucose breakdown
Pyruvate is the end product of glycolysis. In the mitochondrion pyruvate dehydrogenase converts it with coenzyme A. Source 4↕ both, depending on amount Pyruvate stands at a junction: with coenzyme A it becomes acetyl-CoA for energy production; if this step runs slowly, more of it becomes lactate.
established physiology Source 4
⚖ When the balance tips
too much — If pyruvate builds up in front of pyruvate dehydrogenase, more of it is converted to lactate and alanine.
too little — If little pyruvate forms, acetyl-CoA comes more from the breakdown of fatty acids.
established physiology · Source 4
- Fatty acid — from food or fat stores
Fatty acids from food or adipose tissue enter the cells. Before they are broken down or incorporated, they must be attached to coenzyme A. Source 2, 5↑ supplies Fatty acids are a large energy store: their breakdown in the mitochondrion supplies a great deal of acetyl-CoA and electrons for the respiratory chain.
established physiology Source 5
⚖ When the balance tips
too much — If many fatty acids enter the cell, those not broken down are stored as fats.
too little — If few arrive, the cell draws its energy more from sugar.
established physiology · Source 5
Cofactors in this pathway
- Cysteine — Supplies the sulphur group of coenzyme A to which acyl residues are bound Source 2
- Carnitine — Carries fatty acids activated on coenzyme A into the mitochondrion and absorbs surplus acyl groups Source 5In the ORY catalogue as a laboratory value: Carnitin
- NAD⁺ — Accepts the electrons in pyruvate dehydrogenase when acetyl-CoA forms Source 4In the ORY catalogue as a laboratory value: NAD⁺ (Nicotinamidadenindinukleotid)
- TPP (vitamin B1) — Cofactor of pyruvate dehydrogenase that splits pyruvate before coenzyme A receives the acetyl group Source 4
- ATP — Supplies phosphate and the AMP part of coenzyme A and drives the activation of fatty acids Source 2
- Sodium — Flows into the cell together with pantothenic acid through the transporter SMVT Source 1
Sources
- Said HM, Nexo E. Gastrointestinal Handling of Water-Soluble Vitamins. Compr Physiol 2018 · PubMed 30215865
- Czumaj A, Szrok-Jurga S, Hebanowska A et al. The Pathophysiological Role of CoA. Int J Mol Sci 2020 · PubMed 33260564
- Srinivasan B, Sibon OC. Coenzyme A, more than 'just' a metabolic cofactor. Biochem Soc Trans 2014 · PubMed 25110005
- Patel MS, Nemeria NS, Furey W et al. The pyruvate dehydrogenase complexes: structure-based function and regulation. J Biol Chem 2014 · PubMed 24798336
- Longo N, Frigeni M, Pasquali M. Carnitine transport and fatty acid oxidation. Biochim Biophys Acta 2016 · PubMed 26828774
Related pathways
- Carnitine — acyl-coa
- Trans fatty acids — acyl-coa
- Ketone bodies — Carnitin, NAD⁺ (Nicotinamidadenindinukleotid)
- Triglycerides — Carnitin, NAD⁺ (Nicotinamidadenindinukleotid)
As of 2026-10-05. Draft written by Claude to schema v2; sources checked in PubMed; expert review pending
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