Lipoproteins

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Lipoproteins consist of a hydrophobic core and a hydrophilic shell

Lipoproteins (more precisely plasma lipoprotein particles ; formerly also lipoproteins ) are non-covalent aggregates ( proteids ) of lipids and proteins , the micelle-like particles with a non-polar core of cholesterol esters and triacylglycerides as well as a shell with polar, hydrophilic components facing the aqueous phase form, consisting of protein, phospholipids and the hydroxy groups unesterified cholesterol .

function

Plasma lipoprotein particles are used in all animal classes to transport water-insoluble lipids (fats) as well as cholesterol and cholesteryl esters in the blood . Basically, all particles contain both triglycerides and cholesterol and cholesteryl esters, but in very different amounts.

Plasma lipoprotein particles are produced in very specific cells, released into the blood and have a half-life of just a few days. Both its shell and its contents are prone to radical oxidation and there is some evidence that the oxidative modification of low density lipoprotein is an important step in the pathogenesis of atherosclerosis .

In order to release or absorb the respective transported substance, they dock to specific receptor proteins of the target cells by means of their apoproteins.

classification

Lipoproteins, as can be seen from the English names, are largely differentiated on the basis of their physical density, the difference being essentially due to the different protein and lipid content of the respective lipoprotein. Isolation and characterization of the various lipoproteins is accordingly traditionally carried out using density gradient ultracentrifugation , in which a subdivision into six classes has been established, with some additional subclasses:

First there are the relatively large chylomicrons , then the VLDL and the resulting temporary IDL as well as LDL (all three also summarized as beta lipoproteins ) , lipoprotein a and finally HDL, which is now divided into 5 further subclasses (also known as alpha lipoprotein ) .

The isolation of human LDL (which is the focus of arteriosclerosis research) from human blood plasma is possible by ultracentrifugation (centrifugation time: 2 hours; rotor speed: 60,000 revolutions / minute) and is described in detail in the literature references cited.

Separation or characterization of lipoproteins is also possible using other methods, such as electrophoresis .

According to function

Plasma lipoprotein particles
  • Chylomicrons are presumably only formed in the cells of the intestinal wall. Their main function is to transport triglycerides from the intestine (or the intestinal wall) into the blood and from there to the liver, muscle and fat cells.
  • Very Low Density Lipoproteins (VLDL) are only formed in the liver cells and mainly transport triglycerides (stored there and newly synthesized) from the liver cells to the rest of the body cells.
  • Intermediate Density Lipoproteins (IDL) are temporary degradation products of VLDL that are between the VLDL and LDL in terms of size and are therefore normally not detectable in the blood.
  • Lipoprotein a is a component of blood lipids that is very similar in structure to LDL.
  • Low Density Lipoproteins (LDL) are formed in the liver cells and mainly transport cholesterol or cholesteryl esters from the liver to the rest of the body's cells. You can continue this class in
    • small dense LDL small dense LDL particles and
    • large buoyant LDL Divide large buoyant LDL particles
  • High density lipoproteins (HDL) are also made in liver cells, but they mainly carry cholesterol from the rest of the body back into the liver, and they are also able to couple to LDL particles and some of the in those particles to take over transported cholesterol and cholesteryl ester, but also to exchange triglycerides with them.

According to density

The following table lists the mammalian lipoproteins with some of their sub-forms:

Lipoprotein Diameter (nm) Apolipoproteins Concentration
in men (g / l) 		Concentration
in women (g / l)
Chylomicrons <1000 ApoB-48, ApoA-I & II, ApoC-II & III, ApoE <0.1 <0.1
VLDL - V ery L ow D ensity L ipoprotein 50 ApoB-100, ApoC-II, ApoE 0.5-2.0 0.5-1.5
IDL - I ntermediate D ensity L ipoprotein 30th ApoB-100, ApoC-II, ApoE
Lipoprotein a - Lp (a) 25th ApoB-100, Apo (a) 0.01-0.5 0.01-0.5
LDL - L ow D ensity L ipoprotein 21st ApoB-100 2.0-3.5 2.0-3.0
HDL - H igh D ensity L ipoprotein
  HDL E 12 ApoA-I & II <0.05 <0.05
  HDL 1 10 ApoA-I & II, C, E 0.5-1.0 0.5-1.0
  HDL 2 10 ApoA-I & II, C, E 0.5-1.0 0.5-1.0
  HDL 3 8th ApoA-I & II 1.0-2.0 1.0-2.0
  VHDL - V ery H igh D ensity L ipoprotein 7th 0.1-0.2 0.1-0.2

Cholesterol and triglycerides supplied with food are absorbed by the intestinal tract and then released into venous blood in the form of chylomicrons via the lymphatic pathway via the thoracic duct . After the action of lipases remaining and delivery of the released fatty acids in peripheral muscle and fat cells known as chylomicron Remnants (engl. Remnants ) are finally of the liver was added and disassembled.

VLDL, like its metabolites IDL and especially LDL, transport the body's own synthesized cholesterol and the triglycerides taken over by the chylomicrons from the liver to the peripheral tissues. HDL (more precisely HDL 3 ) take up cholesterol with the mediation of the enzyme lecithin cholesterol acyltransferase (LCAT) from the tissues, but also from other lipoproteins, and transport it back to the liver ( reverse cholesterol transport ). The cholesterol transported in the lipoproteins is mainly esterified with fatty acids.

Over 75% of the carbon and hydrogen in energy-supplying substrates in metabolism are lipid components.

The transport proteins are called apolipoproteins (ApoLp). They give the lipid micelles stability and determine the rate of turnover in the metabolism of the lipidoproteins and direct them to specific target organs.

Fat metabolism disorders can be detected via lipoproteins in the blood. The so-called lipoprotein a (Lp (a), pronounced: lipoprotein small "a" ) is a risk factor because it correlates with the occurrence of heart attacks .

For the qualitative and quantitative determination of the lipid fractions of the lipoproteins, chromatographic methods such as. B. thin-layer chromatography and gas chromatography are also used in conjunction with mass spectrometry .

See also

Historical literature

  • Fritz A. Pezold (Ed.): Lipids and lipoproteins in blood plasma. Biochemistry, pathophysiology, clinic. Springer-Verlag, Berlin / Heidelberg / New York 1961.

Web links

Individual evidence

  1. ↑ Hans-Dieter Jakubke, Hans Jeschkeit: amino acids, peptides, proteins , Verlag Chemie, Weinheim, p. 388, 1982, ISBN 3-527-25892-2 .
  2. ↑ D. Steinberg, S. Parthasarathy, TE Carew, JC Khoo, JL Witztum: Beyond Cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity . In: New England Journal of Medicine . tape 320 , no. 14 , 1989, pp. 915-924 , doi : 10.1056 / NEJM198904063201407 , PMID 2648148 .
  3. ↑ Andreas Giessauf, Ernst Steiner, Hermann Esterbauer: Early destruction of tryptophan residues of apolipoprotein B is a vitamin E-independent process during copper-mediated oxidation of LDL . In: Biochimica et Biophysica Acta - Lipids and Lipid Metabolism . tape 1256 , no. 2 , 1995, p. 221-232 , doi : 10.1016 / 0005-2760 (95) 00024-7 .
  4. ↑ Gieseg SP and Waeg G. (1994) Beckman Report 37, issue 77, p. 6
  5. ↑ Blood lipids and elevated blood lipid levels - overview. Retrieved June 19, 2017 .
  6. ↑ B. Rehlender: Qualitative and quantitative determination of lipid fractions of various nutritionally relevant lipoproteins from human sera, analyzes of Extrelut lipid extracts through the combined use of thin-layer chromatography, gas chromatography and mass spectrometry , dissertation TU Berlin, 1983 DNB 840626266
  7. ↑ Lizenko MV, Regerand TI, Bakhirev AM, Petrovskiĭ VI, Lizenko EI: Content of the main lipid components in blood serum lipoproteins of human and of various animal species ] Zh Evol Biokhim Fiziol. 2007 Mar-Apr; 43 (2): 155-61. Russian. PMID 17674708
  8. ^ Ooi EM, Watts GF, Barrett PH, Chan DC, Clifton PM, Ji J, Nestel PJ: Dietary plant sterols supplementation does not alter lipoprotein kinetics in men with the metabolic syndrome . Asia Pac J Clin Nutr. 2007; 16 (4): 624-31. PMID 18042521