Linolsäure (Omega-6): the pathway in the body · Biomarker & Blood Analysis

Linolsäure (Omega-6) is part of the pathway “Omega-6 fatty acids and eicosanoids”. This page shows the whole pathway; the station of Linolsäure (Omega-6) is highlighted.

Where this laboratory value sits: Linoleic acid — omega-6 from food. Linoleic acid is an omega-6 fatty acid from plant oils. The body cannot make it itself; it is the starting material for the longer omega-6 fatty acids. It competes with omega-3 for the same enzymes. Source 1

In brief

Omega-6 fatty acids such as linoleic acid and arachidonic acid are polyunsaturated fatty acids and building blocks of cell membranes. From released arachidonic acid, cells form eicosanoids, short-lived messengers such as prostaglandins and leukotrienes. EPA uses the same enzymes.

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. Linoleic acid → γ-Linolenic acid FADS2 (Δ6-desaturase) · NADH, Oxygen Delta-6 desaturase inserts a further double bond into the chain. The same enzyme also processes omega-3 fatty acids, so the two families compete for it. Omega-3 and omega-6 claim this step at the same time. Source 1↑ supplies GLA is an intermediate: the elongase ELOVL5 lengthens it to DGLA. The step leading to it via Δ6-desaturase is claimed by omega-3 and omega-6 fatty acids at the same time. established physiology Source 1
   ⚖ When the balance tips

   too much — If a lot of GLA forms, the elongase ELOVL5 lengthens more of it to DGLA.

   too little — If Δ6-desaturase is occupied by omega-3 fatty acids or works slowly, little GLA forms, and less arrives further down the route.

   established physiology · Source 1

2. γ-Linolenic acid → Dihomo-γ-linolenic acid ELOVL5 (elongase) An elongase adds two carbon atoms to the chain, forming dihomo-γ-linolenic acid. It is the direct precursor of arachidonic acid. Source 1↑ supplies DGLA is the direct precursor of arachidonic acid; the Δ5-desaturase FADS1 inserts the fourth double bond into it. established physiology Source 1
   ⚖ When the balance tips

   too much — If DGLA builds up, the following Δ5-desaturase sets how much of it becomes arachidonic acid.

   too little — If little DGLA is available, little arachidonic acid forms via the body's own route as well.

   established physiology · Source 1

3. Dihomo-γ-linolenic acid → Arachidonic acid FADS1 (Δ5-desaturase) · NADH, Oxygen Delta-5 desaturase inserts the fourth double bond, forming arachidonic acid. It also comes directly from animal foods. It is the raw material of the omega-6 eicosanoids. Source 1↑ supplies Arachidonic acid is the raw material of the eicosanoids of the omega-6 series. Before cells convert it for this, it is built into the phospholipids of the membranes. established physiology Source 1, 2
   ⚖ When the balance tips

   too much — If a lot of arachidonic acid arrives, more of it is built into membranes, and after a stimulus more starting material for eicosanoids is ready.

   too little — If little arachidonic acid is available and EPA sits in the membranes, cyclooxygenases and lipoxygenases convert proportionally more EPA.

   established physiology · Source 2, 6

4. Arachidonic acid → In the cell membrane Arachidonic acid is built into the phospholipids of cell membranes. Most of it stays there until a stimulus reaches the cell. The membrane thus serves as a store. Source 2↑ supplies The membrane is the store: arachidonic acid sits at the sn-2 position of the phospholipids, where cPLA2 cuts it out selectively. While bound, it does not yet serve as a precursor of messengers. established physiology Source 2
   ⚖ When the balance tips

   too much — If a lot of arachidonic acid sits in the phospholipids, cPLA2 can release more of it after a stimulus.

   too little — If less arachidonic acid and more EPA sit there, proportionally more EPA is released after a stimulus.

   established physiology · Source 2, 6

5. Free arachidonic acid → PGH₂ COX-1, COX-2 · Oxygen, Haem The cyclooxygenases COX-1 and COX-2 add oxygen and form a ring. PGH₂ is formed via the intermediate PGG₂. Prostaglandins and thromboxane arise from PGH₂. Source 3↑ supplies PGH₂ is the common, short-lived precursor of the prostaglandins and of thromboxane A₂. Which synthase a cell has determines what it becomes. established physiology Source 3
   ⚖ When the balance tips

   too much — If a lot of PGH₂ forms, the synthases of the cell concerned convert more of it into their product, in platelets into thromboxane A₂.

   too little — If the cyclooxygenases are inhibited or have too little oxygen, little PGH₂ forms; then fewer prostaglandins and less thromboxane A₂ form as well.

   established physiology · Source 3

6. Free arachidonic acid → LTA₄ 5-Lipoxygenase · FLAP, Calcium 5-lipoxygenase moves with calcium to the nuclear membrane and works there with the helper protein FLAP. LTA₄ is formed via the intermediate 5-HPETE. LTA₄ is the precursor of the leukotrienes. Source 4↑ supplies LTA₄ is a short-lived epoxide and the precursor of two leukotriene families: LTA₄ hydrolase turns it into LTB₄, LTC₄ synthase with glutathione into LTC₄. established physiology Source 4, 5
   ⚖ When the balance tips

   too much — If a lot of LTA₄ forms, the enzymes of the cell determine whether more LTB₄ or more cysteinyl leukotrienes arise from it.

   too little — If 5-lipoxygenase does not reach the nuclear membrane without FLAP or calcium, little LTA₄ forms, and both leukotriene families stay small.

   established physiology · Source 4, 5

7. PGH₂ → Prostaglandins Synthases Tissue-specific synthases turn PGH₂ into various prostaglandins. They break down quickly and therefore act only close to where they are made. PGI₂, for example, relaxes vascular muscle. Source 3↑ supplies Prostaglandins bind to their own receptors on the same or neighbouring cells. PGI₂, for example, relaxes vascular muscle and keeps platelets apart, as the counterpart of thromboxane A₂. established physiology Source 3
   ⚖ When the balance tips

   too much — If many prostaglandins form, they occupy more receptors in the surroundings; because they break down quickly, the effect stays local and brief.

   too little — If little PGH₂ forms, the synthases make few prostaglandins, and their signals to vessels and neighbouring cells become weaker.

   established physiology · Source 3

8. PGH₂ → Thromboxane A₂ Thromboxane synthase In platelets, thromboxane synthase converts PGH₂ into thromboxane A₂. It makes platelets stick together and vascular muscle contract. PGI₂ from the vessel wall counteracts it. Source 3↑ supplies Thromboxane A₂ binds to receptors on platelets and vascular muscle: the platelets stick together, the vessels narrow. PGI₂ from the vessel wall counteracts this. established physiology Source 3
   ⚖ When the balance tips

   too much — If a lot of thromboxane A₂ forms, the platelets stick together more readily, and the balance with PGI₂ shifts towards narrowing.

   too little — If little thromboxane A₂ forms, for instance because more EPA instead of arachidonic acid is converted, platelets stick together less readily; the thromboxane A₃ formed instead acts more weakly.

   observed in studies · Source 3, 6

9. LTA₄ → LTB₄ LTA₄ hydrolase LTA₄ hydrolase turns LTA₄ into leukotriene B₄. It acts as an attractant for white blood cells. The cells then migrate into the tissue. Source 5↑ supplies LTB₄ binds to receptors on neutrophil granulocytes and draws them to where it is formed; the cells attach to vessel walls and migrate into the tissue. established physiology Source 5
   ⚖ When the balance tips

   too much — If a lot of LTB₄ forms, more immune cells migrate into the tissue.

   too little — If little LTB₄ forms, for instance because LTA₄ hydrolase receives little LTA₄, fewer immune cells arrive.

   established physiology · Source 5

10. LTA₄ → Cysteinyl leukotrienes LTC₄ synthase · Glutathione LTC₄ synthase attaches glutathione to LTA₄. This gives rise in turn to LTC₄, LTD₄ and LTE₄, which act on smooth muscle and blood vessels. Smooth muscle contracts in the process. Source 4, 5↑ supplies Cysteinyl leukotrienes bind to their own receptors: smooth muscle, for example in the airways, contracts, and blood vessels become more permeable. established physiology Source 4, 5
    ⚖ When the balance tips

    too much — If many cysteinyl leukotrienes form, smooth muscle contracts more strongly, and more fluid passes from the vessels into the tissue.

    too little — If little glutathione or LTA₄ is available, LTC₄ synthase makes little LTC₄, and hardly any LTD₄ and LTE₄ form either.

    established physiology · Source 4, 5

11. EPA → Eicosanoids from EPA COX, lipoxygenases When COX and lipoxygenases convert EPA, series-3 prostaglandins and series-5 leukotrienes are formed. They bind to the same receptors but act more weakly there. In this way they displace the stronger messengers. Source 6↓ depletes Eicosanoids from EPA occupy the same receptors as those from arachidonic acid but trigger a weaker signal there. Thromboxane A₃ hardly acts on platelets, LTB₅ attracts immune cells more weakly. observed in studies Source 6
    ⚖ When the balance tips

    too much — If many eicosanoids from EPA form, more receptors are occupied by weaker-acting messengers.

    too little — If few form, almost only eicosanoids from arachidonic acid occupy the receptors.

    observed in studies · Source 6

Further stations

• Linoleic acid — omega-6 from food Linoleic acid is an omega-6 fatty acid from plant oils. The body cannot make it itself; it is the starting material for the longer omega-6 fatty acids. It competes with omega-3 for the same enzymes. Source 1↑ supplies Linoleic acid is the starting material for GLA, DGLA and arachidonic acid. At Δ6-desaturase it competes with the omega-3 fatty acid ALA; the more linoleic acid arrives, the more enzyme sites it occupies. established physiology Source 1
  ⚖ When the balance tips

  too much — If a lot of linoleic acid arrives, it occupies more sites on Δ6-desaturase; omega-3 fatty acids are then converted less often.

  too little — If little linoleic acid is available, the body's own route gets little starting material; arachidonic acid then comes more directly from animal foods.

  established physiology · Source 1

• Free arachidonic acid — released after a stimulus When calcium rises in the cell, the phospholipase cPLA2 moves to the membrane and cuts out arachidonic acid. Only as a free molecule is it converted further. It is the substrate of COX and 5-lipoxygenase. Source 2↑ supplies Free arachidonic acid is the substrate of two routes: COX-1 and COX-2 make PGH₂ from it, 5-lipoxygenase makes LTA₄. How much is released is set by cPLA2 and thus by calcium in the cell. established physiology Source 2, 3, 4
  ⚖ When the balance tips

  too much — If a lot of arachidonic acid is released, cyclooxygenases and 5-lipoxygenase get more substrate, and more eicosanoids form.

  too little — If calcium in the cell does not rise, cPLA2 stays in the cytoplasm; then hardly any arachidonic acid is released, and COX and 5-lipoxygenase have little substrate.

  established physiology · Source 2

• EPA — omega-3 fatty acid EPA is built into the same membranes as arachidonic acid and processed by the same enzymes. The ratio of the two in the membrane determines which molecule is converted more often. In this way EPA slows the turnover of arachidonic acid. Source 6↓ depletes EPA partly displaces arachidonic acid from the membrane phospholipids and occupies the same enzymes. As a result, less arachidonic acid is converted to eicosanoids. observed in studies Source 6
  ⚖ When the balance tips

  too much — If there is a lot of EPA in the membranes, less arachidonic acid is released and converted; less thromboxane A₂ and LTB₄ form.

  too little — If little EPA is available, cyclooxygenases and lipoxygenases convert almost only arachidonic acid.

  observed in studies · Source 6

Cofactors in this pathway

• Iron — Haem iron in the cyclooxygenases COX-1 and COX-2; non-haem iron in 5-lipoxygenase; without iron, no conversion Source 3, 4In the ORY catalogue as a laboratory value: Eisen
• Calcium — Guides cPLA2 and 5-lipoxygenase to the membranes where arachidonic acid is released; this starts the conversion Source 2, 4In the ORY catalogue as a laboratory value: Calcium (intrazellulär)
• Glutathione — Attached to LTA₄ by LTC₄ synthase, forming the cysteinyl leukotrienes; they act on smooth muscle Source 4, 5In the ORY catalogue as a laboratory value: Glutathion (GSH)
• NADH — Electron donor for the desaturases FADS1 and FADS2, which insert double bonds; without NADH the synthesis stalls Source 1

Sources

1. Brenna JT, Kothapalli KSD. New understandings of the pathway of long-chain polyunsaturated fatty acid biosynthesis. Curr Opin Clin Nutr Metab Care 2022 · PubMed 34937850
2. Leslie CC. Regulation of the specific release of arachidonic acid by cytosolic phospholipase A2. Prostaglandins Leukot Essent Fatty Acids 2004 · PubMed 15041029
3. Smith WL, DeWitt DL, Garavito RM. Cyclooxygenases: structural, cellular, and molecular biology. Annu Rev Biochem 2000 · PubMed 10966456
4. Peters-Golden M, Brock TG. 5-lipoxygenase and FLAP. Prostaglandins Leukot Essent Fatty Acids 2003 · PubMed 12895592
5. Wan M, Tang X, Stsiapanava A et al. Biosynthesis of leukotriene B4. Semin Immunol 2017 · PubMed 29042025
6. Calder PC. Marine omega-3 fatty acids and inflammatory processes: Effects, mechanisms and clinical relevance. Biochim Biophys Acta 2015 · PubMed 25149823

Whole pathway: Omega-6 fatty acids and eicosanoids

Related pathways

• Omega-3 fatty acids — epa
• Nitrosative stress — Eisen, Calcium (intrazellulär)
• 8-OHdG — Eisen, Glutathion (GSH)
• Calprotectin — Eisen, Calcium (intrazellulär)
• Granulocytes in the gut wall — Eisen, Calcium (intrazellulär)

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