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Triglycerides: the pathway in the body · Biomarker & Blood Analysis

This page shows the biochemical pathway behind the laboratory value Triglycerides: 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

Triglycerides are fats made of three fatty acids and one glycerol, taken in with food or made in the liver. Chylomicrons and VLDL carry them in the blood to muscle and adipose tissue. There lipoprotein lipase releases fatty acids for energy or storage.

11 stations · 6 sources
ORYUptakeTransport in the bloodLipoprotein lipaseApolipoprotein C-IIMTPApolipoprotein B-100Lipoprotein lipasePancreatic lipaseBile acidsColipaseMGAT, DGATMTPApolipoprotein B-48CD36, FATPLDL receptor, LRP1Apolipoprotein Evia the lymph into the bloodOrlistatDietary fattriglyceridesFatty acids releasedin the small intestineTriglycerides againin the gut cellChylomicronstransport spheres for fatChylomicron in bloodloaded with triglyceridesFree fatty acidson the inner vessel wallMuscle and fat tissueuptake of fatty acidsChylomicron remnantwhat is left overLiverhub for fatsVLDLlipoprotein from the liverLDLformed via IDL

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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. Dietary fat → Fatty acids released Pancreatic lipase · Bile acids, Colipase Bile acids break fat into fine droplets. Pancreatic lipase splits off two of the three fatty acids, leaving a monoglyceride. The protein colipase holds the enzyme on the droplet. Only then can they be dissolved in micelles and absorbed. Source 1↑ supplies Only once split do fatty acids and monoglyceride form small micelles with bile acids, which carry them through the watery layer to the gut wall. established physiology Source 1
    ⚖ When the balance tips

    too much — If many fatty acids are released at once, correspondingly many bile acids are needed to dissolve them in micelles; uptake then follows the pace at which micelles form.

    too little — If little lipase or bile acid is present, less fat is split and dissolved; unsplit fat leaves the gut unchanged, as described for the inhibition of lipases by orlistat.

    established physiology · Source 1, 6

  2. Fatty acids released → Triglycerides again MGAT, DGAT Fatty acids and monoglyceride enter the cells of the gut wall. There the enzymes MGAT and DGAT reassemble them into triglycerides. This keeps the amount of free fatty acids in the cell low. Source 1, 2↑ supplies Reassembly into triglycerides keeps the amount of free fatty acids in the gut cell low and so maintains the gradient along which more fatty acids flow in from the gut lumen. established physiology Source 1, 2
    ⚖ When the balance tips

    too much — If MGAT and DGAT build more triglycerides than MTP can package, the gut cell stores them as droplets and releases them later.

    too little — If MGAT and DGAT work more slowly, more free fatty acids remain in the gut cell, and uptake from the gut lumen slows; this is described mainly in animal models.

    observed in studies · Source 1, 2

  3. Triglycerides again → Chylomicrons MTP · Apolipoprotein B-48 The protein MTP loads apolipoprotein B-48 with fat. This forms chylomicrons, which the gut cell releases into the lymph; from there they reach the blood. Without MTP the gut cell cannot release fat. Source 2↑ supplies Chylomicrons make water-insoluble fat transportable in the blood: a coat of protein and phospholipids surrounds the fat core. Without MTP and ApoB-48 the gut cell cannot release fat. established physiology Source 2
    ⚖ When the balance tips

    too much — If a lot of fat arrives, the gut cell makes larger chylomicrons carrying more fat per particle.

    too little — If MTP is barely active, fat accumulates in the gut cell, and less fat and fewer fat-soluble vitamins reach the blood.

    established physiology · Source 2

  4. Chylomicron in blood → Free fatty acids Lipoprotein lipase · Apolipoprotein C-II Lipoprotein lipase sits on the inner wall of small vessels and splits the fatty acids off the triglycerides. Apolipoprotein C-II switches the enzyme on. ApoC-III and ANGPTL proteins slow it down. Source 3↑ supplies The released fatty acids are fuel for muscle and heart and material for the fat stores. ApoC-III and ANGPTL proteins slow lipoprotein lipase and so steer which tissue receives fat when. established physiology Source 3
    ⚖ When the balance tips

    too much — If more fatty acids are released than the local tissue absorbs, part of them enters the circulation bound to albumin and reaches the liver.

    too little — If lipoprotein lipase is slowed, fewer fatty acids are released; triglycerides remain in chylomicrons and VLDL, and muscle and adipose tissue receive less fat from the blood.

    established physiology · Source 3, 4

  5. Free fatty acids → Muscle and fat tissue CD36, FATP Muscle cells feed the fatty acids into β-oxidation and gain energy from them. Fat cells rebuild triglycerides from them and store them in droplets. Adipose tissue releases them again during fasting. Source 3, 5↑ supplies In muscle the fatty acid enters the mitochondrion with carnitine and is broken down there to acetyl-CoA; this yields NADH and FADH₂ for the respiratory chain. In adipose tissue it is stored for times of fasting. established physiology Source 5, 3
    ⚖ When the balance tips

    too much — If more fat arrives than the muscle breaks down, mainly the adipose tissue absorbs the fatty acids and stores them as triglycerides; after meals ANGPTL proteins direct lipoprotein lipase there.

    too little — If little fat arrives from the blood, the fat cells split their stored triglycerides again and release fatty acids for the muscle.

    established physiology · Source 3

  6. Chylomicron in blood → Chylomicron remnant What remains is a smaller particle in which cholesterol predominates. The liver recognises it by apolipoprotein E and absorbs it. It brings dietary cholesterol to the liver. Source 4↑ supplies The remnant brings cholesterol and fat-soluble vitamins from food to the liver. It is absorbed as soon as ApoE binds to the LDL receptor or to LRP1. established physiology Source 4
    ⚖ When the balance tips

    too much — If remnants stay in the blood longer because their uptake into the liver stalls, more cholesterol-rich particles circulate in the blood.

    too little — If few remnants form, for instance because little dietary fat arrives, less dietary cholesterol reaches the liver as well.

    established physiology · Source 4

  7. Chylomicron remnant → Liver LDL receptor, LRP1 · Apolipoprotein E The liver absorbs chylomicron remnants and free fatty acids and makes triglycerides from them again. In this way it balances the supply of fat. Source 4↑ supplies The liver balances the supply: when fat comes in from outside, it packages it into VLDL; between meals it also uses fatty acids for energy and for ketone bodies. established physiology Source 4, 5
    ⚖ When the balance tips

    too much — If more fatty acids arrive in the liver than it breaks down or releases in VLDL, it stores triglycerides in its own droplets.

    too little — If few fatty acids arrive, the liver makes fewer triglycerides and releases less VLDL.

    established physiology · Source 4

  8. Liver → VLDL MTP · Apolipoprotein B-100 Using apolipoprotein B-100 and the protein MTP, the liver packages triglycerides into VLDL particles and releases them into the blood. It supplies the tissues with fat between meals as well. Source 4↑ supplies VLDL carries triglycerides from the liver to muscle and adipose tissue, also between meals; after each release to lipoprotein lipase the particle becomes smaller and richer in cholesterol. established physiology Source 4
    ⚖ When the balance tips

    too much — If the liver releases more VLDL, it uses the same lipoprotein lipase as the chylomicrons, and both stay in the blood longer.

    too little — If the liver releases little VLDL, for instance because MTP is barely active, it retains more triglycerides itself, and less LDL forms in the blood.

    established physiology · Source 3, 4

  9. VLDL → LDL Lipoprotein lipase VLDL also gives up fatty acids to lipoprotein lipase and becomes smaller. Via the intermediate IDL, the remaining particles become cholesterol-rich LDL. It carries mainly cholesterol. Source 4↑ supplies LDL carries hardly any triglycerides but mainly cholesterol, which it delivers to cells via the LDL receptor. It is the end point of the path the triglycerides began in VLDL. established physiology Source 4
    ⚖ When the balance tips

    too much — If more LDL forms from VLDL than the LDL receptors absorb, it stays in the blood longer.

    too little — If little LDL forms, for instance because the liver releases little VLDL, cells obtain more of their cholesterol from their own synthesis.

    established physiology · Source 4

Further stations

Cofactors in this pathway

What acts on this pathway

Sources

  1. Iqbal J, Hussain MM. Intestinal lipid absorption. Am J Physiol Endocrinol Metab 2009 · PubMed 19158321
  2. Hussain MM. Intestinal lipid absorption and lipoprotein formation. Curr Opin Lipidol 2014 · PubMed 24751933
  3. Wen Y, Chen YQ, Konrad RJ. The Regulation of Triacylglycerol Metabolism and Lipoprotein Lipase Activity. Adv Biol (Weinh) 2022 · PubMed 35676229
  4. Feingold KR, Adler RA, Ahmed SF et al. Introduction to Lipids and Lipoproteins. Endotext 2000 · PubMed 26247089
  5. Houten SM, Wanders RJ. A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation. J Inherit Metab Dis 2010 · PubMed 20195903
  6. US prescribing information Xenical (Orlistat, DailyMed), section 12.1 Mechanism of Action · Prescribing information

Related pathways

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