Fats ingested with food and broken down and absorbed in the intestine circulate-bound to proteins (protein)-in the blood. These proteins consist of several apoproteins (part of a protein, which consists only of amino acids), which combine with lipid fractions – consisting of cholesterol and cholesterol esters, triglycerides (TG), and phospholipids – to form the lipoproteins (complex of proteins (apolipoproteins) and lipids, which serves to transport hydrophobic lipids in the blood). By means of ultracentrifuge, these lipoproteins can be separated into the following particles (particles) according to their density, or, in the case of lipoprotein electrophoresis (electrophoresis refers to a laboratory test in which electrically charged particles of blood migrate in an electric field), according to their migration speed:
- Chylomicrons – The largest particles with a lipid (fat) content of circa 98-99.5% – transport mainly dietary triglycerides. They are rapidly degraded by lipoprotein lipases. They are formed after food intake and are not detectable in fasting serum under normal conditions. In electrophoresis, they show almost no migration.
- VLDL – “very low density lipoproteins” (translated: lipoproteins of very low density), transport endogenously (“generated inside”) triglycerides formed in the liver and consist of 85-90% lipids. According to their mobility in electrophoresis, they are called pre-ß lipoproteins.
- LDL – “low density lipoproteins”, transport mainly cholesterol and cholesterol esters and contain about 75% lipids. In electrophoresis, they are called β-lipoproteins. They transport the bulk of cholesterol (65-70%).
- HDL – “high density lipoproteins”, (translated: high density lipoproteins), are called α-lipoproteins in electrophoresis. They contain the highest protein content (50%) (especially apolipoprotein-AI, -AII and -E) and the lowest lipid content (also 50%) and transport about 20% of the cholesterol. They initially circulate in the blood as disc-shaped precursors and then, through the uptake of further lipids and apoproteins, mature into spherical structures that can be subdivided into HDL2a, HDL2b and HDL3 depending on their density and protein components. By their ability to absorb lipids, they seem to be able to CHD risk (risk of coronary heart disease, CHD) to reduce.
Dietary fat is converted to chylomicrons after digestion and absorption (ingestion) and transported into the bloodstream via the thoracic duct. In the capillaries, the chylomicrons are rapidly cleaved by lipoprotein lipases, and the fatty acids released are either stored in adipose tissue or oxidized, depending on energy requirements. The remaining chylomicron remnants (also called “chylomicron remnants”) are finally taken up by the liver where they are further processed. The triglycerides and cholesterol esters from the Chylomicron Remnants are either used directly in the liver for energy production or packaged into transporter molecules. Some of the cholesterol is converted to bile acids and excreted, and then most is reabsorbed via the enterohepatic circulation (intestinal-liver circulation). Lipids formed endogenously (“in the body itself”) from excess dietary calories – predominantly from carbohydrates – originate in the liver. These VLDL formed by the liver are released into the bloodstream and taken up by the target organs (muscle/fatty tissue). In the target organs, they are broken down by lipoprotein lipases to fatty acids and used for energy production or, in the case of dietary excess, stored in adipose tissue. Half of the IDL (intermediate density lipoproteins) remaining after cleavage is reabsorbed by the liver, the rest is converted into LDL. The cholesterol-rich LDLs supply the peripheral cells with the essential (vital) basic building block cholesterol, which is either synthesized (produced) in the liver cells or ingested with food. Cholesterol uptake by peripheral cells is controlled by receptors. If the uptake of LDL into the cells is impaired by receptor defects, the LDL are taken up by macrophages and other cells of the RES (reticulohistiocytic system: part of the immune system and the mononuclear phagocytic system, MPS).These macrophages (scavenger cells) then degenerate as so-called foam cells, deposit in the vessel walls and narrow the lumen (cavity) over time. HDL cholesterol is able to take up cholesterol from the vessels – even from pre-existing deposits – and transport it back to the liver (reverse cholesterol transport, RCT) with the aim of excreting the cholesterol; this occurs either directly or after conversion to bile acids. LDL thus play a key role in atherogenesis (formation or development of arteriosclerosis), whereas HDL, in contrast, have an anti-atherogenic effect, as they can take up cholesterol from the cells and release it to the liver. Influence of omega-3 fatty acids on triglyceride levels
Omega-3 fatty acids, especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), inhibit the synthesis and secretion of VLDL (very low density lipoproteins). By increasing lipoprotein lipase activity, more triglycerides (TG) are removed from VLDL, thus promoting VLDL degradation.Daily intake of 1.5-3 g of omega-3 fatty acids (EPA and DHA) can reduce TG levels by 25-30% in a dose-dependent manner. An intake of 5-6 g can reduce TG by up to 60%. This amount of omega-3 fatty acids is hardly manageable in the framework of a fish-rich diet in everyday life, which is why the use of fish oil capsules is recommended. In contrast to animal omega-3 fatty acids, plant omega-3 fatty acids such as alpha-linolenic acid show no effect on TG levels.
