Propionat (Propionsäure): the pathway in the body

Propionat (Propionsäure) is part of the pathway “Gut microbiome”. This page shows the whole pathway; the station of Propionat (Propionsäure) is highlighted.

Where this laboratory value sits: Propionate — goes to the liver. Propionate arises by several routes, for example via succinate. It reaches the liver through the portal vein and serves there as a building block for new glucose. In the succinate route its formation needs vitamin B12. Source 5, 4

In brief

The gut microbiome is the community of bacteria in the large intestine. They ferment dietary fibre, which human enzymes cannot break down, into short-chain fatty acids such as acetate, propionate and butyrate. Butyrate fuels the gut cells; acetate and propionate act as signals.

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. Stool sample → Bacterial DNA Cell lysis In the laboratory, the cell walls are broken open and the DNA is extracted. How well this works for tough cell walls already affects the result at this stage. Source 1
2. Bacterial DNA → 16S rRNA gene Polymerase (PCR) · Primer One gene occurs in all bacteria and yet differs between species: the 16S rRNA gene. A polymerase amplifies a section of it. Source 1
3. 16S rRNA gene → List of taxa Sequencing The sequences are read and compared with a database. This yields a list of the groups found and how often they occur — depending on the section, down to genus, rarely to species. Source 1
4. List of taxa → Shannon index Calculation The Shannon index combines two things in one number: how many groups are present and how evenly they are distributed. It describes a sample; it does not rate it. Source 2
5. List of taxa → Dysbiosis index Calculation A dysbiosis index compares the pattern of selected bacterial groups with that of a reference group and expresses the distance as a number. Which groups are included is set by each laboratory. Source 3
6. Dietary fibre → Short-chain fatty acids Bacterial enzymes Bacteria ferment the fibre without oxygen. This mainly produces three short-chain fatty acids: acetate, propionate and butyrate. They are fuel for the gut cells and a signal for the body. Source 4, 5↑ supplies Short-chain fatty acids are fuel and signal at once: the mucosa absorbs and uses them, receptors pass the signal on, and as acids they lower the pH of the gut contents. established physiology Source 4, 5
   ⚖ When the balance tips

   too much — If many short-chain fatty acids form, the pH in the colon falls; this slows acid-sensitive bacterial groups and shifts the community towards butyrate producers.

   too little — If few short-chain fatty acids form, the gut cells receive less fuel, and the receptors FFAR2 and FFAR3 less often receive the signal by which the body registers fermentation.

   observed in studies · Source 5

7. Short-chain fatty acids → Butyrate Butyrate is formed mainly by bacteria of the genera Faecalibacterium and Roseburia, usually from two acetyl-CoA building blocks. In the gut cell it is mainly fuel. Source 5↑ supplies Butyrate is above all fuel for the colon lining. Part of it acts inside the cell as an inhibitor of histone deacetylases and so changes which genes are read. observed in studies Source 4
   ⚖ When the balance tips

   too much — If a lot of butyrate is formed, the gut cells use most of it themselves; only a little reaches the liver and the rest of the blood via the portal vein.

   too little — If little butyrate is formed, for instance because Faecalibacterium and Roseburia are scarce, the gut cells have less of it as fuel; in animal models without gut bacteria they then run short of energy.

   observed in studies · Source 4, 5, 6

8. Short-chain fatty acids → Propionate Propionate arises by several routes, for example via succinate. It reaches the liver through the portal vein and serves there as a building block for new glucose. In the succinate route its formation needs vitamin B12. Source 5, 4↑ supplies Propionate supplies the liver with carbon for making new glucose and binds to FFAR2 and FFAR3. In the bacterial succinate route its formation needs vitamin B12. established physiology Source 4, 7, 8
   ⚖ When the balance tips

   too much — If a lot of propionate reaches the liver, most of it is used there; only a small part reaches the rest of the body.

   too little — If little vitamin B12 is available in the gut, the step through methylmalonyl-CoA mutase stalls in the succinate route, and this route contributes less propionate.

   observed in studies · Source 4, 8, 5

9. Short-chain fatty acids → Acetate Acetate is the most abundant of the three fatty acids. It enters the blood and is used in tissues as a fuel and as a building block. In the gut, butyrate producers use part of it. Source 4↑ supplies Acetate supplies tissues with acetyl-CoA as fuel and as a building block for fats and cholesterol; in the gut it serves butyrate producers as starting material. Via FFAR2 and FFAR3 it also acts as a signal. established physiology Source 4, 5, 7
   ⚖ When the balance tips

   too much — If there is a lot of acetate in the gut, butyrate-producing bacteria absorb part of it and build it into butyrate via the CoA transferase; this part does not enter the blood.

   too little — If little acetate is formed, butyrate producers are short of part of their starting material, and less acetate from the gut is available to the tissues.

   observed in studies · Source 5, 4

10. Butyrate → Energy for colon cells β-oxidation · NAD⁺ The cells of the colon lining burn butyrate in their mitochondria; it is their main source of energy. The oxygen used in the process keeps the gut contents low in oxygen. If little butyrate arrives, they run short of energy. Source 6↑ supplies In the mitochondria, butyrate supplies NADH for the respiratory chain via β-oxidation, and thus ATP. In animal models it covers most of the energy needs of colon cells. observed in studies Source 6
    ⚖ When the balance tips

    too much — If more butyrate arrives than the mitochondria burn, part of it stays in the cell and inhibits histone deacetylases there; this changes which genes are read.

    too little — If little butyrate arrives, NADH and ATP fall in the gut cells; in animal models without gut bacteria the cells then break down their own components (autophagy) until butyrate arrives again.

    observed in studies · Source 4, 6

11. Propionate → FFAR2/3 receptors Acetate and propionate bind to the receptors FFAR2 and FFAR3 on gut cells, immune cells and nerve endings. Through them, information about what is fermented in the gut reaches the rest of the body. Depending on the cell type, they switch processes on or off. Source 7↕ both, depending on amount FFAR2 and FFAR3 translate the fatty acids into cell signals: in gut cells they trigger the release of the hormones GLP-1 and PYY, in fat cells they slow fat breakdown via Gi proteins. The cell type sets the direction. observed in studies Source 7
    ⚖ When the balance tips

    too much — If many fatty acids bind, the receptors are activated more often; the L cells of the gut release more GLP-1 and PYY, and immune cells change their release of messenger substances.

    too little — If few fatty acids bind, the receptors mostly stay unoccupied; in animal models without FFAR2 or FFAR3, hormone release from the gut and signals to immune cells are weaker.

    observed in studies · Source 7

12. Acetate → FFAR2/3 receptors Acetate and propionate bind to the receptors FFAR2 and FFAR3 on gut cells, immune cells and nerve endings. Through them, information about what is fermented in the gut reaches the rest of the body. Depending on the cell type, they switch processes on or off. Source 7↕ both, depending on amount FFAR2 and FFAR3 translate the fatty acids into cell signals: in gut cells they trigger the release of the hormones GLP-1 and PYY, in fat cells they slow fat breakdown via Gi proteins. The cell type sets the direction. observed in studies Source 7
    ⚖ When the balance tips

    too much — If many fatty acids bind, the receptors are activated more often; the L cells of the gut release more GLP-1 and PYY, and immune cells change their release of messenger substances.

    too little — If few fatty acids bind, the receptors mostly stay unoccupied; in animal models without FFAR2 or FFAR3, hormone release from the gut and signals to immune cells are weaker.

    observed in studies · Source 7

Further stations

• Stool sample — snapshot of the colon A stool sample contains bacteria from the colon and their genetic material. It mainly reflects what lives in the gut lumen, less so what sits in the mucus layer. Source 1
• Dietary fibre — undigested in the colon Dietary fibre reaches the colon intact: human enzymes cannot split its bonds, but many gut bacteria can. Which kinds arrive helps determine which bacterial groups grow. Source 4↑ supplies Dietary fibre is the starting material for fermentation in the colon. Which kinds arrive, and how much, determines which bacterial groups grow and how many short-chain fatty acids form. established physiology Source 4
  ⚖ When the balance tips

  too much — If a lot of fibre arrives, more is fermented, and the acids formed lower the pH in the proximal colon; in experiments this favours butyrate-producing groups.

  too little — If little fibre arrives, the fermenting bacteria have little starting material; fewer short-chain fatty acids form, and groups that depend on fibre decline.

  observed in studies · Source 5, 4

Cofactors in this pathway

• Coenzyme A — Butyrate is built from two acetyl-CoA units; the intermediates are bound to CoA; at the end CoA is released again Source 5
• Acetate — Taken up by a CoA transferase during the formation of butyrate and so withdrawn from the gut contents Source 5
• Vitamin B12 — Cofactor of methylmalonyl-CoA mutase in the succinate route to propionate; with little of it, this step stalls Source 8
• NAD⁺ — Accepts hydrogen when butyrate is broken down in the gut cells and passes it on to the respiratory chain Source 6In the ORY catalogue as a laboratory value: NAD⁺ (Nicotinamidadenindinukleotid)

Sources

1. Johnson JS, Spakowicz DJ et al. Evaluation of 16S rRNA gene sequencing for species and strain-level microbiome analysis. Nat Commun 2019 · PubMed 31695033
2. Kers JG, Saccenti E. The Power of Microbiome Studies: Some Considerations on Which Alpha and Beta Metrics to Use and How to Report Results. Front Microbiol 2021 · PubMed 35310396
3. Casén C, Vebø HC et al. Deviations in human gut microbiota: a novel diagnostic test for determining dysbiosis in patients with IBS or IBD. Aliment Pharmacol Ther 2015 · PubMed 25973666
4. Koh A, De Vadder F et al. From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites. Cell 2016 · PubMed 27259147
5. Louis P, Flint HJ. Formation of propionate and butyrate by the human colonic microbiota. Environ Microbiol 2017 · PubMed 27928878
6. Donohoe DR, Garge N et al. The microbiome and butyrate regulate energy metabolism and autophagy in the mammalian colon. Cell Metab 2011 · PubMed 21531334
7. Kimura I, Ichimura A et al. Free Fatty Acid Receptors in Health and Disease. Physiol Rev 2020 · PubMed 31487233
8. Degnan PH, Taga ME, Goodman AL. Vitamin B12 as a modulator of gut microbial ecology. Cell Metab 2014 · PubMed 25440056

Whole pathway: Gut microbiome

Related pathways

• Gut bacteria — dietary fibre
• Fructose absorption — short-chain fatty acids
• Gut fermentation and breath gases — short-chain fatty acids
• Lactose digestion — short-chain fatty acids

As of 2026-09-16. Draft, written by Claude to schema v2; sources checked in PubMed; expert approval pending
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