Electrophoretic analysis of lipoproteins
Last reviewed: 23.04.2024
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Lipoprotein of blood plasma - the transport form of lipids in the human body. They carry the transport of lipids as exogenous (food), and endogenous origin. Individual lipoproteins capture excess cholesterol from cells of peripheral tissues to transport it to the liver, where it is oxidized to bile acids and excretion with bile. With the participation of lipoproteins are also transported fat-soluble vitamins and hormones.
Plasma lipoproteins have a spherical shape. Inside is a fat "drop" containing nonpolar lipids (triglycerides and esterified cholesterol) and forming the core of the LP particle. It is surrounded by a shell of phospholipids, unesterified cholesterol and protein.
There are several methods for determining lipoproteins in the blood. One of them - the determination of the cholesterol content in various classes of lipoproteins - is discussed above. Another method of studying the content of lipoproteins is electrophoretic. Using this method, individual fractions of lipoproteins are classified by comparing their electrophoretic mobility with the mobility of conventional whey proteins. Based on electrophoretic mobility, lipoproteins were divided into the following fractions.
- Chylomicrons. When electrophoresis is performed, chylomicrons remain at the start (contain very little protein) like y-globulins; are fat-rich particles entering the blood from lymph and transporting triglycerides. They are the largest lipoproteins. Plasma of blood of healthy people who did not take food for 12-14 hours, chylomicrons does not contain or contains them in insignificant amounts.
- Alpha lipoproteins. With electrophoresis, a-LPs move together with alpha globulins and correspond to HDL. HDL contains up to 50% protein, about 30% phospholipids, 20% cholesterol and very few triglycerides. Formed in the liver and small intestine wall.
- Beta-lipoproteins. When electrophoresis on paper, the beta-LP moves along with beta-globulins and correspond to LDL. LDL contains 25% of protein, 50% of cholesterol, 20% of phospholipids and 8-10% of triglycerides. It is suggested that LDL is formed partially or completely during the breakdown of very low density lipoproteins (VLDL).
- Pre-beta-lipoproteins. With electrophoresis, pre-beta-lipoproteins are between alpha-lipoproteins and beta-lipoproteins, they correspond to VLDL.
Electrophoresis of lipoproteins allows a qualitative analysis of lipoproteins. There are two metabolic processes that determine the pathogenesis of atherosclerosis: the rate of infiltration of the rich cholesterol in the inner layer of the blood vessel wall and the rate of removal of cholesterol from the vessels with subsequent excretion from the body. In this balanced system, elevated concentrations of chylomicrons, VLDL and LDL determine the risk of excess cholesterol deposition inside the vessel wall. On the other hand, increased HDL concentrations contribute to an increase in cholesterol removal rate from atherosclerotic plaques. The LP electrophoresis method can provide additional information on the relationship of these metabolic processes.
In addition to the classes of lipoproteins listed above, other PL-complexes, including unusual ones, which are called pathological (or conditionally pathological) LP, can be detected in the blood plasma. These include β-VLDL, HDL- x and LP-X. β-VLDL, also referred to as flotation β-LP, is characterized by having the electrophoretic mobility inherent in β-LP and the density corresponding to VLDL, due to which they float with ultracentrifugation together with the latter. The presence of β-VLDL is a characteristic feature of type III DLP. HDL cholesterol is the fraction of HDL cholesterol overloaded, the role of the PL are not elucidated in the pathogenesis of atherosclerosis. LP-X is characterized by a high content of phospholipids (65-68%) and unesterified cholesterol (23-27%). Due to their high rigidity, LP-X helps increase the viscosity of the blood. They appear in the blood with obstructive jaundice and in the absence of lecithin-cholesterol acyltransferase. The role of LP-X in the development of atherosclerosis has not been studied.
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