– a group of heterogeneous chemical structure and physical and chemical properties of substances. In blood serum they are represented mainly by fatty acids, triglycerides, cholesterol and phospholipids.
Triglycerides are the main form of lipid storage in adipose tissue and lipid transport in the blood. A study of triglyceride levels is necessary to determine the type of hyperlipoproteinemia and assess the risk of developing cardiovascular diseases.
Cholesterol performs essential functions: part of cell membranes, is a precursor bile acids, steroid hormones and vitamin D, acts as an antioxidant. About 10% of the Russian population have increased level cholesterol in the blood. This condition is asymptomatic and can lead to serious illnesses(atherosclerotic vascular lesions, coronary disease hearts).
Lipids are insoluble in water, so they are transported by blood serum in combination with proteins. Lipid+protein complexes are called lipoproteins. And proteins that are involved in lipid transport are called apoproteins.
Several classes are present in blood serum lipoproteins: chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL).
Each lipoprotein fraction has its own function. synthesized in the liver and transport mainly triglycerides. Play an important role in atherogenesis. Low-density lipoproteins (LDL) rich in cholesterol, deliver cholesterol to peripheral tissues. Levels of VLDL and LDL promote the deposition of cholesterol in the vascular wall and are considered atherogenic factors. High density lipoproteins (HDL) participate in the reverse transport of cholesterol from tissues, taking it away from overloaded tissue cells and transferring it to the liver, which “utilizes” it and removes it from the body. High HDL level is considered as an antiatherogenic factor (protects the body from atherosclerosis).
The role of cholesterol and the risk of developing atherosclerosis depends on which lipoprotein fractions it is included in. To assess the ratio of atherogenic and antiatherogenic lipoproteins, it is used atherogenic index.
Apolipoproteins- These are proteins that are located on the surface of lipoproteins.
Apolipoprotein A (ApoA protein) is the main protein component of lipoproteins (HDL), which transports cholesterol from peripheral tissue cells to the liver.
Apolipoprotein B (ApoB protein) is part of lipoproteins that transport lipids to peripheral tissues.
Measuring the concentration of apolipoprotein A and apolipoprotein B in blood serum provides the most accurate and unambiguous determination of the ratio of atherogenic and antiatherogenic properties of lipoproteins, which is assessed as the risk of developing atherosclerotic vascular lesions and coronary heart disease over the next five years.
To the study lipid profile includes the following indicators: cholesterol, triglycerides, VLDL, LDL, HDL, atherogenicity coefficient, cholesterol/triglycerides ratio, glucose. This profile gives full information about lipid metabolism, allows you to determine the risks of developing atherosclerotic vascular lesions, coronary heart disease, identify the presence of dyslipoproteinemia and type it, and also, if necessary, select the right lipid-lowering therapy.
Indications
Increased concentrationcholesterol It has diagnostic value with primary familial hyperlipidemia (hereditary forms of the disease); pregnancy, hypothyroidism, nephrotic syndrome, obstructive liver diseases, pancreatic diseases (chronic pancreatitis, malignant neoplasms), diabetes mellitus.
Decreased concentrationcholesterol has diagnostic value for liver diseases (cirrhosis, hepatitis), starvation, sepsis, hyperthyroidism, megaloblastic anemia.
Increased concentrationtriglycerides has diagnostic value for primary hyperlipidemia (hereditary forms of the disease); obesity, excessive consumption carbohydrates, alcoholism, diabetes mellitus, hypothyroidism, nephrotic syndrome, chronic renal failure, gout, acute and chronic pancreatitis.
Decreased concentrationtriglycerides has diagnostic value for hypolipoproteinemia, hyperthyroidism, malabsorption syndrome.
Very low density lipoproteins (VLDL) used to diagnose dyslipidemia (types IIb, III, IV and V). High concentrations of VLDL in the blood serum indirectly reflect the atherogenic properties of the serum.
Increased concentrationlow density lipoprotein (LDL) has diagnostic value for primary hypercholesterolemia, dislipoproteinemia (types IIa and IIb); for obesity, obstructive jaundice, nephrotic syndrome, diabetes mellitus, hypothyroidism. Determination of LDL level is necessary for prescribing long-term treatment, the purpose of which is to reduce lipid concentrations.
Increased concentration has diagnostic value for liver cirrhosis and alcoholism.
Decreased concentrationhigh density lipoprotein (HDL) has diagnostic value for hypertriglyceridemia, atherosclerosis, nephrotic syndrome, diabetes mellitus, acute infections, obesity, smoking.
Level determination apolipoprotein A indicated for early assessment of the risk of coronary heart disease; identifying patients with a hereditary predisposition to atherosclerosis in a relatively at a young age; monitoring treatment with lipid-lowering drugs.
Increased concentrationapolipoprotein A has diagnostic value for liver diseases and pregnancy.
Decreased concentrationapolipoprotein A has diagnostic value for nephrotic syndrome, chronic renal failure, triglyceridemia, cholestasis, sepsis.
Diagnostic valueapolipoprotein B- the most accurate indicator of the risk of developing cardiovascular diseases, is also the most adequate indicator of the effectiveness of statin therapy.
Increased concentrationapolipoprotein B has diagnostic value for dyslipoproteinemia (IIa, IIb, IV and V types), coronary heart disease, diabetes mellitus, hypothyroidism, nephrotic syndrome, liver diseases, Itsenko-Cushing syndrome, porphyria.
Decreased concentrationapolipoprotein B has diagnostic value for hyperthyroidism, malabsorption syndrome, chronic anemia, inflammatory diseases joints, multiple myeloma.
Methodology
The determination is carried out on the “Architect 8000” biochemical analyzer.
Preparation
to study the lipid profile (cholesterol, triglycerides, HDL-C, LDL-C, Apo-proteins of lipoproteins (Apo A1 and Apo-B)
It is necessary to refrain from physical activity, drinking alcohol, smoking and medicines, dietary changes for at least two weeks before blood collection.
Blood is taken only on an empty stomach, 12-14 hours after the last meal.
Preferably morning reception medicines carry out after drawing blood (if possible).
The following procedures should not be performed before donating blood: injections, punctures, general body massage, endoscopy, biopsy, ECG, X-ray examination, especially with the introduction of a contrast agent, dialysis.
If there was still minor physical activity, you need to rest for at least 15 minutes before donating blood.
Lipid testing is not performed when infectious diseases, since there is a decrease in the level of total cholesterol and HDL-C, regardless of the type of infectious agent or the clinical condition of the patient. Lipid profile should be checked only after full recovery patient.
It is very important that these recommendations are strictly followed, since only in this case will reliable blood test results be obtained.
Studies of lipid and lipoprotein (LP) metabolism, cholesterol (CH), unlike others diagnostic tests, are of social importance, as they require urgent measures to prevent cardiovascular diseases. The problem of coronary atherosclerosis has shown a clear clinical significance of each biochemical indicator as a risk factor for coronary heart disease (CHD), and in the last decade, approaches to assessing disorders of lipid and lipoprotein metabolism have changed.The risk of developing atherosclerotic vascular lesions is assessed using the following biochemical tests:
Determination of TC/HDL-C, LDL-C/HDL-C ratios.
Triglycerides
TG are neutral insoluble lipids that enter the plasma from the intestine or liver.
In the small intestine, TGs are synthesized from exogenous ones supplied with food. fatty acids, glycerol and monoacylglycerols.
The formed TGs initially enter lymphatic vessels, then in the form of chylomicrons (CM) through the thoracic lymphatic duct enter the bloodstream. The lifetime of chemical substances in plasma is short; they enter the fat depots of the body.
The presence of CM explains the whitish color of plasma after eating a fatty meal. ChMs are quickly released from TGs with the participation of lipoprotein lipase (LPL), leaving them in adipose tissues. Normally, after a 12-hour fast, CMs are not detected in plasma. Due to the low protein content and high amount of TG, CMs remain at the starting line in all types of electrophoresis.
Along with TGs supplied with food, endogenous TGs are formed in the liver from endogenously synthesized fatty acids and triphosphoglycerol, the source of which is carbohydrate metabolism. These TGs are transported by the blood to the body's fat depots as part of very low-density lipoproteins (VLDL). VLDL is the main transport form of endogenous TG. The content of VLDL in the blood correlates with an increase in TG levels. When VLDL levels are high, the blood plasma appears cloudy.
To study TG, blood serum or plasma is used after a 12-hour fast. Storage of samples is possible for 5-7 days at a temperature of 4 °C; repeated freezing and thawing of samples is not allowed.
Cholesterol
XC is integral part all cells of the body. It is part of cell membranes, LP, and is a precursor of steroid hormones (mineral and glucocorticoids, androgens and estrogens).
CS is synthesized in all cells of the body, but the bulk of it is formed in the liver and comes with food. The body synthesizes up to 1 g of cholesterol per day.
CS is a hydrophobic compound, the main form of transport of which in the blood is protein-lipid micellar complexes of drugs. Their surface layer is formed by hydrophilic heads of phospholipids, apolipoproteins; esterified cholesterol is more hydrophilic than cholesterol, therefore cholesterol esters move from the surface to the center of the lipoprotein micelle.
The bulk of cholesterol is transported in the blood in the form of LDL from the liver to peripheral tissues. The apolipoprotein of LDL is apo-B. LDL interacts with apo B receptors plasma membranes cells are taken up by them through endocytosis. The cholesterol released in cells is used to build membranes and is esterified. CS from the surface of cell membranes enters a micellar complex consisting of phospholipids, apo-A, and forms HDL. The cholesterol in HDL undergoes esterification under the action of lecithin cholesterol acyl transferase (LCAT) and enters the liver. In the liver, cholesterol received as part of HDL undergoes microsomal hydroxylation and is converted into bile acids. It is excreted both in bile and in the form of free cholesterol or its esters.
A study of cholesterol levels does not provide diagnostic information about a specific disease, but characterizes the pathology of lipid and lipid metabolism. The highest levels of cholesterol occur with genetic disorders of lipid metabolism: familial homo- and heterozygous hypercholesterolemia, familial combined hyperlipidemia, polygenic hypercholesterolemia. In a number of diseases, secondary hypercholesterolemia develops: nephrotic syndrome, diabetes mellitus, hypothyroidism, alcoholism.
To assess the state of lipid and lipid metabolism, the values of total cholesterol, TG, HDL cholesterol, VLDL cholesterol, and LDL cholesterol are determined.
Determining these values allows you to calculate the atherogenicity coefficient (Ka):
Ka = TC - HDL cholesterol / VLDL cholesterol,
And other indicators. For calculations, you also need to know the following proportions:
VLDL cholesterol = TG (mmol/l) /2.18; LDL cholesterol = TC – (HDL cholesterol + VLDL cholesterol).
They have different densities and are indicators of lipid metabolism. There are various methods quantification total lipids: colorimetric, nephelometric.
Principle of the method. The hydrolysis products of unsaturated lipids form a red compound with the phosphovanillin reagent, the color intensity of which is directly proportional to the content of total lipids.
Most lipids are not found in the blood free state, and as part of protein-lipid complexes: chylomicrons, α-lipoproteins, β-lipoproteins. Lipoproteins can be divided various methods: centrifugation in saline solutions various densities, electrophoresis, thin layer chromatography. During ultracentrifugation, chylomicrons and lipoproteins of different densities are isolated: high (HDL - α-lipoproteins), low (LDL - β-lipoproteins), very low (VLDL - pre-β-lipoproteins), etc.
Lipoprotein fractions differ in the amount of protein, the relative molecular weight of the lipoproteins, and the percentage of individual lipid components. Thus, α-lipoproteins, containing a large amount of protein (50-60%), have a higher relative density (1.063-1.21), while β-lipoproteins and pre-β-lipoproteins contain less protein and a significant amount of lipids - up to 95% of the total relative molecular weight and low relative density (1.01-1.063).
Principle of the method. When serum LDL interacts with the heparin reagent, turbidity appears, the intensity of which is determined photometrically. Heparin reagent is a mixture heparin with calcium chloride.
Material under study: blood serum.
Reagents: 0.27% CaCl 2 solution, 1% heparin solution.
Equipment: micropipette, FEC, cuvette with an optical path length of 5 mm, test tubes.
PROGRESS. Add 2 ml of a 0.27% CaCl 2 solution and 0.2 ml of blood serum into a test tube and mix. Determine the optical density of the solution (E 1) against a 0.27% CaCl 2 solution in cuvettes using a red filter (630 nm). The solution from the cuvette is poured into a test tube, 0.04 ml of a 1% heparin solution is added with a micropipette, mixed, and exactly 4 minutes later, the optical density of the solution (E 2) is determined again under the same conditions.
The difference in optical density is calculated and multiplied by 1000 - an empirical coefficient proposed by Ledvina, since constructing a calibration curve is associated with a number of difficulties. The answer is expressed in g/l.
x(g/l) = (E 2 - E 1) 1000.
. The content of LDL (b-lipoproteins) in the blood varies depending on age, gender and is normally 3.0-4.5 g/l. An increase in LDL concentration is observed in atherosclerosis, obstructive jaundice, acute hepatitis, chronic diseases liver, diabetes, glycogenosis, xanthomatosis and obesity, decreased in b-plasmocytoma. The average LDL cholesterol content is about 47%.
Determination of total cholesterol in blood serum based on the Liebermann-Burkhard reaction (Ilk method)
Exogenous cholesterol in the amount of 0.3-0.5 g comes from food products, and endogenous is synthesized in the body in an amount of 0.8-2 g per day. Especially a lot of cholesterol is synthesized in the liver, kidneys, adrenal glands, and arterial wall. Cholesterol is synthesized from 18 molecules of acetyl-CoA, 14 molecules of NADPH, 18 molecules of ATP.
When acetic anhydride and concentrated sulfuric acid are added to blood serum, the liquid turns successively red, blue and finally green color. The reaction is caused by the formation of green sulfonic acid cholesterylene.
Reagents: Liebermann-Burkhard reagent (ice-cold mixture) acetic acid, acetic anhydride and concentrated sulfuric acid in a ratio of 1:5:1), standard (1.8 g/l) cholesterol solution.
Equipment: dry test tubes, dry pipettes, FEC, cuvettes with an optical path length of 5 mm, thermostat.
PROGRESS. All test tubes, pipettes, cuvettes must be dry. You need to be very careful when working with the Liebermann-Burkhard reagent. 2.1 ml of Liebermann-Burkhard reagent is placed in a dry test tube, 0.1 ml of non-hemolyzed blood serum is added very slowly along the wall of the test tube, the test tube is shaken vigorously, and then thermostated for 20 minutes at 37ºC. An emerald green color develops, which is colorimeterized on FEC with a red filter (630-690 nm) against the Liebermann-Burkhard reagent. The optical density obtained on the FEC is used to determine the cholesterol concentration according to the calibration graph. The found cholesterol concentration is multiplied by 1000, since 0.1 ml of serum is taken into the experiment. The conversion factor to SI units (mmol/l) is 0.0258. Normal content total cholesterol (free and esterified) in blood serum 2.97-8.79 mmol/l (115-340 mg%).
Building a calibration graph. From a standard cholesterol solution, where 1 ml contains 1.8 mg of cholesterol, take 0.05; 0.1; 0.15; 0.2; 0.25 ml and adjusted to a volume of 2.2 ml with the Liebermann-Burkhard reagent (2.15; 2.1; 2.05; 2.0; 1.95 ml, respectively). The amount of cholesterol in the sample is 0.09; 0.18; 0.27; 0.36; 0.45 mg. The resulting standard cholesterol solutions, as well as the test tubes, are shaken vigorously and placed in a thermostat for 20 minutes, after which they are photometered. The calibration graph is constructed based on the extinction values obtained as a result of photometry of standard solutions.
Clinical and diagnostic value. If lipid metabolism is disrupted, cholesterol can accumulate in the blood. An increase in cholesterol levels in the blood (hypercholesterolemia) is observed when atherosclerosis , diabetes mellitus, obstructive jaundice, jade , nephrosis(especially lipoid nephrosis), hypothyroidism. A decrease in blood cholesterol (hypocholesterolemia) is observed with anemia, fasting, tuberculosis , hyperthyroidism, cancer cachexia, parenchymal jaundice, central nervous system damage, febrile conditions, upon administration
Pyruvic acid in the blood
Clinical and diagnostic significance of the study
Normal: 0.05-0.10 mmol/l in the blood serum of adults.
Contents of the PVK increases in hypoxic conditions caused by severe cardiovascular, pulmonary, cardiorespiratory failure, anemia, with malignant neoplasms, acute hepatitis and other liver diseases (most pronounced in the terminal stages of liver cirrhosis), toxicosis, insulin-dependent diabetes mellitus, diabetic ketoacidosis, respiratory alkalosis, uremia, hepatocerebral dystrophy, hyperfunction of the pituitary-adrenal and sympathetic-adrenal systems, as well as administration of camphor, strychnine , adrenaline and during heavy physical exertion, tetany, convulsions (with epilepsy).
Clinical and diagnostic value of determining the content of lactic acid in the blood
Lactic acid(MK) is the end product of glycolysis and glycogenolysis. A significant amount of it is formed in muscles. From muscle tissue MK travels through the bloodstream to the liver, where it is used for glycogen synthesis. At the same time, part of the lactic acid from the blood is absorbed by the heart muscle, which utilizes it as an energy material.
SUA level in blood increases in hypoxic conditions, acute purulent inflammatory tissue damage, acute hepatitis, liver cirrhosis, renal failure, malignant neoplasms, diabetes mellitus (approximately 50% of patients), mild degree uremia, infections (especially pyelonephritis), acute septic endocarditis, poliomyelitis, serious illnesses blood vessels, leukemia, intense and prolonged muscle stress, epilepsy, tetany, tetanus, convulsive states, hyperventilation, pregnancy (in the third trimester).
Lipids are substances of various chemical structures that have a number of common physical, physicochemical and biological properties. They are characterized by the ability to dissolve in ether, chloroform, and other fatty solvents and only slightly (and not always) in water, and also form, together with proteins and carbohydrates, the main structural component of living cells. The inherent properties of lipids are determined by characteristic features the structures of their molecules.
The role of lipids in the body is very diverse. Some of them serve as a form of deposition (triacylglycerols, TG) and transport (free fatty acids-FFA) of substances, the breakdown of which releases a large amount of energy, others are the most important structural components cell membranes (free cholesterol and phospholipids). Lipids take part in the processes of thermoregulation, protecting vital organs (for example, kidneys) from mechanical stress (trauma), protein loss, and creating elasticity skin, protecting them from excessive moisture removal.
Some of the lipids are biologically active substances, having the properties of modulators of hormonal effects (prostaglandins) and vitamins (polyunsaturated fatty acids). Moreover, lipids promote absorption fat-soluble vitamins A,D,E,K; act as antioxidants ( vitamins A, E), largely regulating the process of free radical oxidation of physiologically important compounds; determine the permeability of cell membranes to ions and organic compounds.
Lipids serve as precursors for a number of steroids with pronounced biological effects - bile acids, vitamins D, sex hormones, and adrenal hormones.
The concept of “total lipids” in plasma includes neutral fats (triacylglycerols), their phosphorylated derivatives (phospholipids), free and ester-bound cholesterol, glycolipids, and non-esterified (free) fatty acids.
Clinical and diagnostic value determination of the level of total lipids in blood plasma (serum)
The norm is 4.0-8.0 g/l.
Hyperlipidemia (hyperlipemia) – an increase in the concentration of total plasma lipids as physiological phenomenon can be observed 1.5 hours after eating. Nutritional hyperlipemia is more pronounced, the lower the level of lipids in the patient’s blood on an empty stomach.
The concentration of lipids in the blood changes under a number of pathological conditions. Thus, in patients with diabetes mellitus, along with hyperglycemia, pronounced hyperlipemia is observed (often up to 10.0-20.0 g/l). With nephrotic syndrome, especially lipoid nephrosis, the content of lipids in the blood can reach even higher numbers - 10.0-50.0 g/l.
Hyperlipemia – constant phenomenon in patients with biliary cirrhosis and in patients with acute hepatitis (especially in the icteric period). Elevated levels of lipids in the blood are usually found in individuals suffering from acute or chronic nephritis, especially if the disease is accompanied by edema (due to the accumulation of LDL and VLDL in the plasma).
The pathophysiological mechanisms that cause changes in the content of all fractions of total lipids, to a greater or lesser extent, determine a pronounced change in the concentration of its constituent subfractions: cholesterol, total phospholipids and triacylglycerols.
Clinical and diagnostic significance of the study of cholesterol (CH) in blood serum (plasma)
A study of cholesterol levels in blood serum (plasma) does not provide accurate diagnostic information about a specific disease, but only reflects the pathology of lipid metabolism in the body.
According to the data epidemiological studies, the upper level of cholesterol in the blood plasma is almost healthy people at the age of 20-29 years it is 5.17 mmol/l.
In blood plasma, cholesterol is found mainly in LDL and VLDL, with 60-70% of it in the form of esters (bound cholesterol), and 30-40% in the form of free, non-esterified cholesterol. Bound and free cholesterol make up the total cholesterol.
High risk The development of coronary atherosclerosis in people aged 30-39 and over 40 years old occurs at cholesterol levels exceeding 5.20 and 5.70 mmol/l, respectively.
Hypercholesterolemia is the most proven risk factor for coronary atherosclerosis. This has been confirmed by numerous epidemiological and clinical studies who established a connection between hypercholesterolemia and coronary atherosclerosis, the incidence of coronary artery disease and myocardial infarction.
Most high level cholesterol is observed in genetic disorders in lipid metabolism: familial homo-heterozygous hypercholesterolemia, familial combined hyperlipidemia, polygenic hypercholesterolemia.
In a number of pathological conditions, secondary hypercholesterolemia develops . It is observed in liver diseases, kidney damage, malignant tumors pancreas and prostate, gout, ischemic heart disease, acute heart attack myocardium, hypertension, endocrine disorders, chronic alcoholism, glycogenosis type I, obesity (in 50-80% of cases).
A decrease in plasma cholesterol levels is observed in patients with malnutrition, with damage to the central nervous system, mental retardation, chronic failure of cardio-vascular system, cachexia, hyperthyroidism, acute infectious diseases, acute pancreatitis, acute purulent-inflammatory processes in soft tissues, febrile conditions, pulmonary tuberculosis, pneumonia, respiratory sarcoidosis, bronchitis, anemia, hemolytic jaundice, acute hepatitis, malignant liver tumors, rheumatism.
Determination of the fractional composition of cholesterol in blood plasma and its individual lipids (primarily HDL) has acquired great diagnostic importance for judging the functional state of the liver. According to modern concepts, the esterification of free cholesterol into HDL occurs in the blood plasma thanks to the enzyme lecithin-cholesterol acyltransferase, which is formed in the liver (this is an organ-specific liver enzyme). The activator of this enzyme is one of the basic components of HDL - apo-Al, which is constantly synthesized in the liver.
A nonspecific activator of the plasma cholesterol esterification system is albumin, also produced by hepatocytes. This process primarily reflects functional state liver. If normally the coefficient of cholesterol esterification (ᴛ.ᴇ. the ratio of the content of ether-bound cholesterol to total) is 0.6-0.8 (or 60-80%), then in case of acute hepatitis, exacerbation chronic hepatitis͵ liver cirrhosis, obstructive jaundice, as well as chronic alcoholism, it decreases. A sharp decrease in the severity of the cholesterol esterification process indicates insufficiency of liver function.
Clinical and diagnostic significance of studying the concentration of total phospholipids in blood serum.
Phospholipids (PL) are a group of lipids containing, in addition to phosphoric acid (as an essential component), alcohol (usually glycerol), fatty acid residues and nitrogenous bases. Taking into account the dependence on the nature of the alcohol, PLs are divided into phosphoglycerides, phosphosphingosines and phosphoinositides.
The level of total PL (lipid phosphorus) in blood serum (plasma) increases in patients with primary and secondary hyperlipoproteinemia types IIa and IIb. This increase is most pronounced in glycogenosis type I, cholestasis, obstructive jaundice, alcoholic and biliary cirrhosis, viral hepatitis(mild course), renal coma, posthemorrhagic anemia, chronic pancreatitis, severe diabetes mellitus, nephrotic syndrome.
To diagnose a number of diseases, it is more informative to study the fractional composition of serum phospholipids. To this end, in last years Lipid thin layer chromatography methods are widely used.
Composition and properties of blood plasma lipoproteins
Almost all plasma lipids are associated with proteins, which gives them good solubility in water. These lipid-protein complexes are commonly referred to as lipoproteins.
According to modern concepts, lipoproteins are high-molecular water-soluble particles, which are complexes of proteins (apoproteins) and lipids formed by weak, non-covalent bonds, in which polar lipids (PL, CXC) and proteins (“apo”) form a surface hydrophilic monomolecular layer surrounding and protecting the internal phase (consisting mainly of ECS, TG) from water.
In other words, LP are peculiar globules, inside of which there is a fat drop, a core (formed predominantly by non-polar compounds, mainly triacylglycerols and cholesterol esters), delimited from water by a surface layer of protein, phospholipids and free cholesterol.
The physical characteristics of lipoproteins (their size, molecular weight, density), as well as the manifestations of physicochemical, chemical and biological properties, largely depend, on the one hand, on the ratio between the protein and lipid components of these particles, on the other hand, on the composition of the protein and lipid components, ᴛ.ᴇ. their nature.
The largest particles, consisting of 98% lipids and a very small (about 2%) proportion of protein, are chylomicrons (CM). Οʜᴎ are formed in the cells of the mucous membrane of the small intestine and are a transport form for neutral dietary fats, ᴛ.ᴇ. exogenous TG.
Table 7.3 Composition and some properties of serum lipoproteins (Komarov F.I., Korovkin B.F., 2000)
| Criteria for assessing individual classes of lipoproteins | HDL (alpha-LP) | LDL (beta-LP) | VLDL (pre-beta-LP) | HM |
| Density, kg/l | 1,063-1,21 | 1,01-1,063 | 1,01-0,93 | 0,93 |
| Molecular weight of drug, kD | 180-380 | 3000- 128 000 | - | |
| Particle sizes, nm | 7,0-13,0 | 15,0-28,0 | 30,0-70,0 | 500,0 - 800,0 |
| Total proteins, % | 50-57 | 21-22 | 5-12 | |
| Total lipids, % | 43-50 | 78-79 | 88-95 | |
| Free cholesterol, % | 2-3 | 8-10 | 3-5 | |
| Esterified cholesterol, % | 19-20 | 36-37 | 10-13 | 4-5 |
| Phospholipids, % | 22-24 | 20-22 | 13-20 | 4-7 |
| Triacylglycerols,% | ||||
| 4-8 | 11-12 | 50-60 | 84-87 |
If exogenous TGs are transported into the blood by chylomicrons, then the transport form endogenous triglycerides are VLDL. Their formation is a protective reaction of the body aimed at preventing fatty infiltration, and subsequently liver degeneration.
The size of VLDL is on average 10 times smaller than the size of CM (individual VLDL particles are 30-40 times smaller than CM particles). They contain 90% of lipids, of which more than half are TG. 10% of all plasma cholesterol is carried by VLDL. Due to the content of a large amount of TG, VLDL shows insignificant density (less than 1.0). Determined that LDL and VLDL contain 2/3 (60%) of all cholesterol plasma, while 1/3 is HDL.
HDL– the densest lipid-protein complexes, since the protein content in them is about 50% of the mass of the particles. Their lipid component consists half of phospholipids, half of cholesterol, mainly ether-bound. HDL is also constantly formed in the liver and partly in the intestines, as well as in the blood plasma as a result of the “degradation” of VLDL.
If LDL and VLDL deliver Cholesterol from the liver to other tissues(peripheral), including vascular wall, That HDL transports cholesterol from cell membranes (primarily the vascular wall) to the liver. In the liver it goes to the formation of bile acids. In accordance with this participation in cholesterol metabolism, VLDL and themselves LDL are called atherogenic, A HDL– antiatherogenic drugs. Atherogenicity is usually understood as the ability of lipid-protein complexes to introduce (transmit) free cholesterol contained in the drug into tissues.
HDL competes with LDL for cell membrane receptors, thereby counteracting the utilization of atherogenic lipoproteins. Since the surface monolayer of HDL contains a large amount of phospholipids, at the point of contact of the particle with outer membrane endothelial, smooth muscle and any other cells create favorable conditions for the transfer of excess free cholesterol to HDL.
In this case, the latter remains in the surface HDL monolayer only for a very short time, since with the participation of the LCAT enzyme it undergoes esterification. The formed ECS, being a nonpolar substance, moves into the internal lipid phase, releasing vacancies to repeat the act of capturing a new ECS molecule from the cell membrane. From here: the higher the activity of LCAT, the more effective the antiatherogenic effect of HDL, which are considered as LCAT activators.
When the balance between the processes of the influx of lipids (cholesterol) into the vascular wall and their outflow from it is disturbed, conditions are created for the formation of lipoidosis, the most famous manifestation of which is atherosclerosis.
In accordance with the ABC nomenclature of lipoproteins, primary and secondary lipoproteins are distinguished. Primary LPs are formed by any apoprotein of one chemical nature. These include LDL, which contains about 95% apoprotein B. All others are secondary lipoproteins, which are associated complexes of apoproteins.
Normally, approximately 70% of plasma cholesterol is found in “atherogenic” LDL and VLDL, while about 30% circulates in “antiatherogenic” HDL. With this ratio in vascular wall(and other tissues) a balance is maintained between the rates of inflow and outflow of cholesterol. This determines the numerical value cholesterol ratio atherogenicity, component of the specified lipoprotein distribution of total cholesterol 2,33 (70/30).
According to the results of mass epidemiological observations, at a concentration of total cholesterol in plasma of 5.2 mmol/l, a zero balance of cholesterol in the vascular wall is maintained. An increase in the level of total cholesterol in the blood plasma of more than 5.2 mmol/l leads to its gradual deposition in the vessels, and at a concentration of 4.16-4.68 mmol/l a negative cholesterol balance is observed in the vascular wall. The level of total cholesterol in blood plasma (serum) exceeding 5.2 mmol/l is considered pathological.
Table 7.4 Scale for assessing the likelihood of developing coronary artery disease and other manifestations of atherosclerosis
(Komarov F.I., Korovkin B.F., 2000)
