Electrophoretic analysis of lipoproteins

Blood plasma lipoprotein is a transport form of lipids in the human body. They transport lipids of both exogenous (food) and endogenous origin. Some lipoproteins capture excess cholesterol from peripheral tissue cells to transport it to the liver, where it is oxidized into bile acids and excreted with bile. Lipid-soluble vitamins and hormones are also transported with the participation of lipoproteins.

Plasma lipoproteins are spherical in shape. Inside is a fat "droplet" containing non-polar lipids (triglycerides and esterified cholesterol) and forming the core of the LP particle. It is surrounded by a shell of phospholipids, non-esterified cholesterol and protein.

There are several methods for determining lipoproteins in the blood. One of them is determining the cholesterol content in various classes of lipoproteins - discussed above. Another method for studying lipoprotein content is electrophoretic. When using this method, individual fractions of lipoproteins are classified by comparing their electrophoretic mobility with the mobility of normal serum proteins. Based on the electrophoretic mobility, lipoproteins were divided into the following fractions.

• Chylomicrons. When conducting electrophoresis, chylomicrons remain at the start (contain very little protein) like y-globulins; they are fat-rich particles that enter the blood from the lymph and transport food triglycerides. They are the largest lipoproteins. The blood plasma of healthy people who have not eaten for 12-14 hours does not contain chylomicrons or contains them in negligible quantities.
• Alpha lipoproteins. During electrophoresis, a-LP move together with alpha globulins and correspond to HDL. HDL contains up to 50% protein, approximately 30% phospholipids, 20% cholesterol and very little triglycerides. They are formed in the liver and the wall of the small intestine.
• Beta lipoproteins. During paper electrophoresis, beta LP move together with beta globulins and correspond to LDL. LDL contains 25% protein, 50% cholesterol, 20% phospholipids and 8-10% triglycerides. It is assumed that LDL is formed partially or completely by the breakdown of very low density lipoproteins (VLDL).
• Pre-beta lipoproteins. During electrophoresis, pre-beta lipoproteins appear between alpha-lipoproteins and beta-lipoproteins, they correspond to VLDL.

Lipoprotein electrophoresis allows for a qualitative analysis of lipoproteins. There are two metabolic processes that determine the pathogenesis of atherosclerosis: the rate of infiltration of cholesterol-rich lipoproteins into the inner layer of the blood vessel wall and the rate of cholesterol removal from the vessels with subsequent elimination from the body. In this balanced system, increased concentrations of chylomicrons, VLDL and LDL determine the risk of excess cholesterol deposition inside the vessel wall. On the other hand, increased concentrations of HDL contribute to an increased rate of cholesterol removal from atherosclerotic plaques. LP electrophoresis can provide additional information on the relationship between these metabolic processes.

In addition to the above-mentioned classes of lipoproteins, other lipoprotein complexes can be found in blood plasma, including unusual ones, which are called pathological (or conditionally pathological) lipoproteins. These include β-VLDL, HDL- _chs and LP-C. β-VLDL, also called floating β-LP, are characterized by having electrophoretic mobility inherent in β-LP and a density corresponding to VLDL, due to which they float during ultracentrifugation together with the latter. The presence of β-VLDL is a characteristic feature of type III DLP. HDL- _chs is a fraction of HDL overloaded with cholesterol; the role of these lipoproteins in the pathogenesis of atherosclerosis has not been clarified. LP-C is characterized by a high content of phospholipids (65-68%) and non-esterified cholesterol (23-27%). Due to their high rigidity, LP-X contribute to an increase in blood viscosity. They appear in the blood during obstructive jaundice and during lecithin-cholesterol acyltransferase deficiency. The role of LP-X in the development of atherosclerosis has not been studied.

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