Study of lipid metabolism. Blood lipid spectrum Determination of total lipids

Studies of the metabolism of lipids and lipoproteins (LP), cholesterol (CS), unlike other 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 approaches to assessing lipid and lipoprotein metabolism disorders have changed in the last decade.

The risk of developing atherosclerotic vascular lesions is assessed by the following biochemical tests:

Determination of the ratios of total cholesterol / cholesterol-HDL, cholesterol-LDL / cholesterol-HDL.

Triglycerides

TG - neutral insoluble lipids that enter the plasma from the intestine or from the liver.

In the small intestine, triglycerides are synthesized from exogenous dietary fatty acids, glycerol and monoacylglycerols.
Formed triglycerides initially enter the lymphatic vessels, then in the form of chylomicrons (CM) through the thoracic lymphatic duct enter the bloodstream. The lifetime of HM in plasma is short, they enter the body's fat depots.

The presence of HM explains the whitish color of the plasma after ingestion of fatty foods. HM are quickly released from TG with the participation of lipoprotein lipase (LPL), leaving them in adipose tissues. Normally, after a 12-hour fast, HM is not detected in plasma. Due to the low protein content and high amount of TG, CM remain on the start line in all types of electrophoresis.

Along with dietary TG, endogenous TG are formed in the liver from endogenously synthesized fatty acids and triphosphoglycerol, the source of which is carbohydrate metabolism. These triglycerides are transported by the blood to the body's fat depots as part of very low density lipoproteins (VLDL). VLDL are the main transport form of endogenous TG. The content of VLDL in the blood correlates with the rise in TG levels. With a high content of VLDL, the blood plasma looks cloudy.

To study TG, blood serum or blood 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

Cholesterol is an integral part of all body cells. It is part of cell membranes, LP, is a precursor of steroid hormones (mineral and glucocorticoids, androgens and estrogens).

Cholesterol is synthesized in all cells of the body, but most 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 LP. 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 main part of cholesterol is transported in the blood in the form of LDL from the liver to peripheral tissues. The LDL apolipoprotein is apo-B. LDL interact with apo-B receptors of plasma membranes of cells, are captured by them by endocytosis. The cholesterol released in the cells is used to build membranes and is esterified. Cholesterol from the surface of cell membranes enters into a micellar complex consisting of phospholipids, apo-A, and forms HDL. HDL cholesterol undergoes esterification under the action of lecithincholesterolacyl transferase (LCAT) and enters the liver. In the liver, HDL-derived cholesterol undergoes microsomal hydroxylation and turns into bile acids. Its excretion occurs both in the composition of bile and in the form of free cholesterol or its esters.

The study of the level of cholesterol does not provide diagnostic information about a specific disease, but characterizes the pathology of lipid and lipid metabolism. The highest numbers of cholesterol occur in genetic disorders of LP 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 LP metabolism, the values of total cholesterol, TG, HDL cholesterol, VLDL cholesterol, LDL cholesterol are determined.

The determination of these values allows you to calculate the coefficient of atherogenicity (Ka):

Ka = total cholesterol - HDL cholesterol / VLDL cholesterol,

And other indicators. For calculations, it is also necessary to know the following proportions:

VLDL cholesterol \u003d TG (mmol / l) / 2.18; LDL cholesterol = total cholesterol - (HDL cholesterol + VLDL cholesterol).

lipids called fats that enter the body with food and are formed in the liver. Blood (plasma or serum) contains 3 main classes of lipids: triglycerides (TG), cholesterol (CS) and its esters, phospholipids (PL).
Lipids are able to attract water, but most of them do not dissolve in the blood. They are transported in a protein-bound state (in the form of lipoproteins or, in other words, lipoproteins). Lipoproteins differ not only in composition, but also in size and density, but their structure is almost the same. The central part (core) is represented by cholesterol and its esters, fatty acids, triglycerides. The shell of the molecule consists of proteins (apoproteins) and water-soluble lipids (phospholipids and non-esterified cholesterol). The outer part of apoproteins is able to form hydrogen bonds with water molecules. Thus, lipoproteins can partially dissolve in fats, partially in water.
Chylomicrons after entering the blood break down into glycerol and fatty acids, resulting in the formation of lipoproteins. Cholesterol-containing residues of chylomicrons are processed in the liver.
From cholesterol and triglycerides in the liver, very low density lipoproteins (VLDL) are formed, which donate part of the triglycerides to peripheral tissues, while their remains return to the liver and are converted into low density lipoproteins (LDL).
LPN II are transporters of cholesterol for peripheral tissues, which is used to build cell membranes and metabolic reactions. In this case, non-esterified cholesterol enters the blood plasma and binds to high-density lipoproteins (HDL). Esterified cholesterol (associated with esters) is converted to VLDL. Then the cycle repeats.
The blood also contains intermediate density lipoproteins (LDL), which are the remains of chylomicrons and VLDL and contain large amounts of cholesterol. LDL in liver cells with the participation of lipase are converted into LDL.
Blood plasma contains 3.5-8 g/l of lipids. An increase in the level of lipids in the blood is called hyperlipidemia, and a decrease is called hypolipidemia. The indicator of total blood lipids does not give a detailed idea of the state of fat metabolism in the body.
Diagnostic value is the quantitative determination of specific lipids. The lipid composition of blood plasma is presented in the table.

Lipid composition of blood plasma

Fraction of lipids		Norm indicator
General lipids		4.6-10.4 mmol/l
Phospholipids		1.95-4.9 mmol/l
Lipid phosphorus		1.97-4.68 mmol/l
Neutral Fats		0-200 mg%
Triglycerides		0.565-1.695 mmol/l (serum)
Non-esterified fatty acids		400-800 mmol/l
Free fatty acids		0.3-0.8 µmol/l
Total cholesterol (there are age norms)		3.9-6.5 mmol/l (unified method)
free cholesterol		1.04-2.33 mmol/l
Cholesterol esters		2.33-3.49 mmol/l
HDL	M	1.25-4.25 g/l
	AND	2.5-6.5 g/l
LDL		3-4.5 g/l

A change in the lipid composition of the blood - dyslipidemia - is an important sign of atherosclerosis or a condition preceding it. Atherosclerosis, in turn, is the main cause of coronary heart disease and its acute forms (angina pectoris and myocardial infarction).
Dyslipidemias are divided into primary, associated with congenital metabolic disorders, and secondary. The causes of secondary dyslipidemia are physical inactivity and overnutrition, alcoholism, diabetes mellitus, hyperthyroidism, cirrhosis of the liver, and chronic renal failure. In addition, they can develop during treatment with glucocorticosteroids, B-blockers, progestins and estrogens. The classification of dyslipidemia is presented in the table.

Classification of dyslipidemias

Type of	An increase in blood levels
Type of	Lipoprotein	lipids
I	Chylomicrons	Cholesterol, triglycerides
On the	LDL	Cholesterol (not always)
Type of	An increase in blood levels
Type of	Lipoprotein	lipids
Nb	LDL, VLDL	Cholesterol, triglycerides
III	VLDL, LPPP	Cholesterol, triglycerides
IV	VLDL	Cholesterol (not always), triglycerides
V	Chylomicrons, VLDL	Cholesterol, triglycerides

Different density and are indicators of lipid metabolism. There are various methods for the quantitative determination of total lipids: colorimetric, nephelometric.

The principle of the method. The hydrolysis products of unsaturated lipids form a red compound with the phosphovaniline reagent, the color intensity of which is directly proportional to the content of total lipids.

Most lipids are found in the blood not in a free state, but as part of protein-lipid complexes: chylomicrons, α-lipoproteins, β-lipoproteins. Lipoproteins can be separated by various methods: centrifugation in saline solutions of various densities, electrophoresis, thin layer chromatography. During ultracentrifugation, chylomicrons and lipoproteins of different density are isolated: high (HDL - α-lipoproteins), low (LDL - β-lipoproteins), very low (VLDL - pre-β-lipoproteins), etc.

Fractions of lipoproteins differ in the amount of protein, the relative molecular weight of 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).

Method principle. When LDL of blood serum interacts with a heparin reagent, turbidity appears, the intensity of which is determined photometrically. The heparin reagent is a mixture of heparin and calcium chloride.

Material under study: blood serum.

Reagents: 0.27% CaCl 2 solution, 1% heparin solution.

Equipment: micropipette, FEK, cuvette with an optical path length of 5 mm, test tubes.

PROGRESS. 2 ml of a 0.27% solution of CaCl 2 and 0.2 ml of blood serum are added to the test tube, mixed. Determine the optical density of the solution (E 1) against a 0.27% CaCl 2 solution in cuvettes with a red light 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 after 4 minutes 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 - the empirical coefficient proposed by Ledvina, since the construction of a calibration curve is associated with a number of difficulties. The answer is expressed in g/l.

x (g / l) \u003d (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 the concentration of LDL is observed in atherosclerosis, obstructive jaundice, acute hepatitis, chronic liver diseases, diabetes, glycogenosis, xanthomatosis and obesity, a decrease in b-plasmocytoma. The average cholesterol content in LDL is about 47%.

Determination of total cholesterol in blood serum based on the Liebermann-Burchard reaction (Ilk method)

Exogenous cholesterol in the amount of 0.3-0.5 g comes with food, and endogenous cholesterol is synthesized in the body in the amount of 0.8-2 g per day. Especially a lot of cholesterol is synthesized in the liver, kidneys, adrenal glands, 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 the blood serum, the liquid turns red, blue, and finally green. The reaction is due to the formation of green sulfonic acid cholesterylene.

Reagents: Liebermann-Burchard reagent (a mixture of glacial 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, FEK, cuvettes with an optical path length of 5 mm, a thermostat.

PROGRESS. All test tubes, pipettes, cuvettes must be dry. It is necessary to work with the Liebermann-Burchard reagent very carefully. 2.1 ml of the Liebermann-Burchard reagent is placed in a dry tube, 0.1 ml of non-hemolyzed blood serum is added very slowly along the wall of the tube, the tube is vigorously shaken, and then thermostated for 20 minutes at 37ºС. An emerald green color develops, which is colorimetric on FEC with a red light filter (630-690 nm) against the Liebermann-Burchard reagent. The optical density obtained on the FEC is used to determine the concentration of cholesterol according to the calibration curve. The found concentration of cholesterol is multiplied by 1000, since 0.1 ml of serum is taken in the experiment. The conversion factor to SI units (mmol/l) is 0.0258. The normal content of total cholesterol (free and esterified) in the blood serum is 2.97-8.79 mmol / l (115-340 mg%).

Construction of a calibration graph. From a standard solution of cholesterol, 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-Burchard reagent (respectively 2.15; 2.1; 2.05; 2.0; 1.95 ml). The amount of cholesterol in the sample is 0.09; 0.18; 0.27; 0.36; 0.45 mg. The obtained standard solutions of cholesterol, as well as experimental test tubes, are vigorously shaken and placed in a thermostat for 20 minutes, after which they are photometered. The calibration graph is built according to the extinction values obtained as a result of photometry of standard solutions.

Clinical and diagnostic value. In violation of fat metabolism, cholesterol can accumulate in the blood. An increase in blood cholesterol (hypercholesterolemia) is observed in atherosclerosis, diabetes mellitus, obstructive jaundice, nephritis, nephrosis (especially lipoid nephrosis), and hypothyroidism. A decrease in blood cholesterol (hypocholesterolemia) is observed with anemia, starvation, tuberculosis, hyperthyroidism, cancer cachexia, parenchymal jaundice, CNS damage, febrile conditions, with the introduction

Pyruvic acid in the blood

Clinical and diagnostic significance of the study

Norm: 0.05-0.10 mmol / l in the blood serum of adults.

PVC content increases in hypoxic conditions caused by severe cardiovascular, pulmonary, cardiorespiratory insufficiency, anemia, 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 the introduction of camphor, strychnine, adrenaline and during heavy physical exertion, tetany, convulsions (with epilepsy).

Clinical and diagnostic significance of determining the content of lactic acid in the blood

Lactic acid(MK) is the end product of glycolysis and glycogenolysis. A significant amount is formed in muscles. From the muscle tissue, MK with the blood flow enters the liver, where it is used for the synthesis of glycogen. 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.

Blood UA level increases with hypoxic conditions, acute purulent inflammatory tissue damage, acute hepatitis, cirrhosis of the liver, renal failure, malignant neoplasms, diabetes mellitus (approximately 50% of patients), mild uremia, infections (especially pyelonephritis), acute septic endocarditis, poliomyelitis, severe diseases blood vessels, leukemia, intense and prolonged muscle exertion, epilepsy, tetany, tetanus, convulsive conditions, hyperventilation, pregnancy (in the third trimester).

Lipids are chemically diverse substances that have a number of common physical, physicochemical and biological properties. Οʜᴎ are characterized by the ability to dissolve in ether, chloroform, other fatty solvents and only slightly (and not always) in water, and also form the main structural component of living cells together with proteins and carbohydrates. The inherent properties of lipids are determined by the characteristic features of the structure 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 decay of which releases a large amount of energy, others are the most important structural components of cell membranes (free cholesterol and phospholipids). Lipids take part in the processes of thermoregulation, protection of vital organs (for example, kidneys) from mechanical influences (injuries), protein loss, in creating elasticity of the skin, protecting them from excessive moisture removal.

Some of the lipids are biologically active substances that have the properties of modulators of hormonal influence (prostaglandins) and vitamins (fatty polyunsaturated acids). Moreover, lipids promote the absorption of 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 in relation to ions and organic compounds.

Lipids serve as precursors for a number of steroids with a pronounced biological effect - bile acids, vitamins of group D, sex hormones, hormones of the adrenal cortex.

The concept of "total lipids" of plasma includes neutral fats (triacylglycerols), their phosphorylated derivatives (phospholipids), free and ester-bound cholesterol, glycolipids, non-esterified (free) fatty acids.

Clinical and diagnostic value determination of the level of total lipids in plasma (serum) of blood

The norm is 4.0-8.0 g / l.

Hyperlipidemia (hyperlipemia) - an increase in the concentration of total plasma lipids as a physiological phenomenon can be observed 1.5 hours after a meal. Alimentary 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 in a number of pathological conditions. So, in patients with diabetes, along with hyperglycemia, there is a pronounced hyperlipemia (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 figures - 10.0-50.0 g / l.

Hyperlipemia is a constant phenomenon in patients with biliary cirrhosis of the liver and in patients with acute hepatitis (especially in the icteric period). Elevated blood lipids are usually found in individuals suffering from acute or chronic nephritis, especially if the disease is accompanied by edema (due to the accumulation of plasma LDL and VLDL).

The pathophysiological mechanisms that cause shifts in the content of all fractions of total lipids determine, to a greater or lesser extent, a pronounced change in the concentration of its constituent subfractions: cholesterol, total phospholipids and triacylglycerols.

Clinical and diagnostic significance of the study of cholesterol (CS) in serum (plasma) of blood

The study of the level of cholesterol in the serum (plasma) of the blood does not provide accurate diagnostic information about a specific disease, but only reflects the pathology of lipid metabolism in the body.

According to epidemiological studies, the upper level of cholesterol in the blood plasma of practically healthy people aged 20-29 years is 5.17 mmol/l.

In blood plasma, cholesterol is found mainly in the composition of LDL and VLDL, with 60-70% of it being 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 amount of total cholesterol.

A high risk of developing coronary atherosclerosis in people aged 30-39 and older than 40 years 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 that have established a link between hypercholesterolemia and coronary atherosclerosis, the incidence of coronary artery disease and myocardial infarction.

The highest level of cholesterol is observed in genetic disorders in the metabolism of LP: 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 of the pancreas and prostate, gout, coronary artery disease, acute myocardial infarction, hypertension, endocrine disorders, chronic alcoholism, type I glycogenosis, 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 insufficiency of the cardiovascular 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.

The determination of the fractional composition of blood plasma cholesterol and its individual lipoproteins (primarily HDL) has become of great diagnostic importance for judging the functional state of the liver. According to the modern view, the esterification of free cholesterol in HDL is carried out in the blood plasma due 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.

Albumin, also produced by hepatocytes, serves as a nonspecific activator of the plasma cholesterol esterification system. This process primarily reflects the functional state of the liver. If the normal coefficient of cholesterol esterification (ᴛ.ᴇ. the ratio of the content of ester-bound cholesterol to total) is 0.6-0.8 (or 60-80%), then in acute hepatitis, exacerbation of chronic hepatitis, liver cirrhosis, obstructive jaundice , as well as chronic alcoholism, it decreases. A sharp decrease in the severity of the process of cholesterol esterification indicates a lack of liver function.

Clinical and diagnostic significance of the study of 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), an alcohol (usually glycerol), fatty acid residues, and nitrogenous bases. Given the dependence on the nature of alcohol, PL is divided into phosphoglycerides, phosphosphingosines, and phosphoinositides.

The level of total PL (lipid phosphorus) in the blood serum (plasma) is increased in patients with primary and secondary hyperlipoproteinemia types IIa and IIb. This increase is most pronounced in type I glycogenosis, cholestasis, obstructive jaundice, alcoholic and biliary cirrhosis, viral hepatitis (mild), renal coma, posthemorrhagic anemia, chronic pancreatitis, severe diabetes mellitus, nephrotic syndrome.

For the diagnosis of a number of diseases, it is more informative to study the fractional composition of blood serum phospholipids. For this purpose, thin-layer lipid chromatography methods have been widely used in recent years.

Composition and properties of blood plasma lipoproteins

Almost all plasma lipids are associated with proteins, which gives them good water solubility. These lipid-protein complexes are commonly referred to as lipoproteins.

According to the modern concept, 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”) make up the 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 mainly by non-polar compounds, mainly triacylglycerols and cholesterol esters), delimited from water by a surface layer of protein, phospholipids and free cholesterol.

The physical features 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 (XM). 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 blood serum lipoproteins (Komarov F.I., Korovkin B.F., 2000)

Criteria for evaluating 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 LP, kD	180-380		3000- 128 000	-
Particle size, 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 TG are transferred into the blood by chylomicrons, then the transport form endogenous TG are VLDL. Their formation is a protective reaction of the body, aimed at preventing fatty infiltration, and subsequently liver dystrophy.

The dimensions of VLDL are on average 10 times smaller than the size of CM (individual particles of VLDL are 30-40 times smaller than CM particles). They contain 90% of lipids, among which more than half of the content is TG. 10% of total plasma cholesterol is carried by VLDL. Due to the content of a large amount of TG VLDL, an insignificant density is detected (less than 1.0). Determined that LDL and VLDL contain 2/3 (60%) of all cholesterol plasma, while 1/3 is accounted for by HDL.

HDL- the most dense lipid-protein complexes, since the protein content in them is about 50% of the particle mass. Their lipid component consists half of phospholipids, half of cholesterol, mainly ester-bound. HDL is also constantly formed in the liver and partly in the intestine, 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, then HDL transport 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 such participation in cholesterol metabolism, VLDL and themselves LDL are called atherogenic, a HDL– antiatherogenic drugs. Under atherogenicity, it is customary to understand the ability of lipid-protein complexes to contribute (transfer) free cholesterol contained in LP into tissues.

HDL compete for cell membrane receptors with LDL, thereby counteracting the utilization of atherogenic lipoproteins. Since the surface monolayer of HDL contains a large amount of phospholipids, favorable conditions are created at the point of contact of the particle with the outer membrane of the endothelial, smooth muscle, and any other cell for the transfer of excess free cholesterol to HDL.

At the same time, the latter lingers in the surface monolayer of HDL only for a very short time, since it undergoes esterification with the participation of the LCAT enzyme. The formed ECS, being a non-polar substance, moves into the internal lipid phase, freeing vacancies for repeating the act of capturing a new CXC molecule from the cell membrane. From here: the higher the activity of LCAT, the more effective the anti-atherogenic effect of HDL, which are considered as LCAT activators.

If the balance between the processes of influx of lipids (cholesterol) into the vascular wall and their outflow from it are 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 one apoprotein by chemical nature. They are conventionally classified as LDL, which contain about 95% of apoprotein-B. All the rest are secondary lipoproteins, which are associated complexes of apoproteins.

Normally, approximately 70% of plasma cholesterol is in the composition of "atherogenic" LDL and VLDL, while about 30% circulates in the composition of "anti-atherogenic" HDL. With this ratio in the vascular wall (and other tissues), the balance of the rates of inflow and outflow of cholesterol is maintained. This determines the numerical value cholesterol coefficient atherogenicity, which, with the indicated 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 balance of cholesterol in the vascular wall is observed. The level of total plasma (serum) cholesterol in excess of 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)

Pyruvic acid in the blood

Clinical and diagnostic significance of the study

Norm: 0.05-0.10 mmol / l in the blood serum of adults.

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 is formed in muscles. From the muscle tissue, MK with the blood flow enters the liver, where it is used for the synthesis of glycogen. In addition, part of the lactic acid from the blood is absorbed by the heart muscle, which utilizes it as an energy material.

Lipids are chemically diverse substances that have a number of common physical, physicochemical and biological properties. They are characterized by the ability to dissolve in ether, chloroform, other fatty solvents and only slightly (and not always) in water, and also form the main structural component of living cells together with proteins and carbohydrates. The inherent properties of lipids are determined by the characteristic features of the structure 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 decay of which releases a large amount of energy, others are the most important structural components of cell membranes (free cholesterol and phospholipids). Lipids are involved in the processes of thermoregulation, protection of vital organs (for example, kidneys) from mechanical influences (injuries), protein loss, in creating elasticity of the skin, protecting them from excessive moisture removal.

Lipids serve as precursors for a number of steroids with a pronounced biological effect - bile acids, vitamins of group D, sex hormones, hormones of the adrenal cortex.

Clinical and diagnostic significance of determining the level of total lipids in blood plasma (serum)

The norm is 4.0-8.0 g / l.

Clinical and diagnostic significance of the study of cholesterol (CS) in serum (plasma) of blood

According to epidemiological studies, the upper level of cholesterol in the blood plasma of practically healthy people aged 20-29 years is 5.17 mmol/l.

A high risk of developing coronary atherosclerosis in people aged 30-39 and older than 40 years occurs at cholesterol levels exceeding 5.20 and 5.70 mmol / l, respectively.

Of great diagnostic importance is the determination of the fractional composition of blood plasma cholesterol and its individual lipoproteins (primarily HDL) for judging the functional state of the liver. According to the modern view, the esterification of free cholesterol in HDL is carried out in the blood plasma due 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 main components of HDL - apo - Al, which is constantly synthesized in the liver.

Albumin, also produced by hepatocytes, serves as a nonspecific activator of the plasma cholesterol esterification system. This process primarily reflects the functional state of the liver. If normally the coefficient of cholesterol esterification (i.e. the ratio of the content of ether-bound cholesterol to total) is 0.6-0.8 (or 60-80%), then in acute hepatitis, exacerbation of chronic hepatitis, cirrhosis of the liver, obstructive jaundice, and also chronic alcoholism, it decreases. A sharp decrease in the severity of the process of cholesterol esterification indicates a lack of liver function.

Clinical and diagnostic significance of the study of 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), an alcohol (usually glycerol), fatty acid residues, and nitrogenous bases. Depending on the nature of the alcohol, PL is subdivided into phosphoglycerides, phosphosphingosines, and phosphoinositides.

The level of total PL (lipid phosphorus) in the blood serum (plasma) is increased in patients with primary and secondary hyperlipoproteinemia types IIa and IIb. This increase is most pronounced in type I glycogenosis, cholestasis, obstructive jaundice, alcoholic and biliary cirrhosis, viral hepatitis (mild course), renal coma, posthemorrhagic anemia, chronic pancreatitis, severe diabetes mellitus, nephrotic syndrome.

Composition and properties of blood plasma lipoproteins

Almost all plasma lipids are associated with proteins, which gives them good water solubility. These lipid-protein complexes are commonly referred to as lipoproteins.

The largest particles, consisting of 98% lipids and a very small (about 2%) proportion of protein, are chylomicrons (XM). They are formed in the cells of the mucous membrane of the small intestine and are a transport form for neutral dietary fats, i.e. exogenous TG.

Table 7.3 Composition and some properties of blood serum lipoproteins (Komarov F.I., Korovkin B.F., 2000)

Criteria for evaluating 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 LP, kD	180-380		3000- 128 000	-
Particle size, 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

The dimensions of VLDL are on average 10 times smaller than the size of CM (individual particles of VLDL are 30-40 times smaller than CM particles). They contain 90% of lipids, among which more than half of the content is TG. 10% of total plasma cholesterol is carried by VLDL. Due to the content of a large amount of TG VLDL, an insignificant density is detected (less than 1.0). Determined that LDL and VLDL contain 2/3 (60%) of the total cholesterol plasma, while 1/3 is accounted for by HDL.

If a LDL and VLDL deliver cholesterol from the liver to other tissues(peripheral), including vascular wall, then HDL transport 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 such participation in cholesterol metabolism, VLDL and themselves LDL are called atherogenic, a HDL– antiatherogenic drugs. Atherogenicity refers to the ability of lipid-protein complexes to introduce (transfer) free cholesterol contained in LP into tissues.

However, the latter is retained in the surface monolayer of HDL only for a very short time, since it undergoes esterification with the participation of the LCAT enzyme. The formed ECS, being a non-polar substance, moves into the internal lipid phase, freeing vacancies for repeating the act of capturing a new CXC molecule from the cell membrane. From here: the higher the activity of LCAT, the more effective the anti-atherogenic effect of HDL, which are considered as LCAT activators.

If the balance between the influx of lipids (cholesterol) into the vascular wall and their outflow from it is disturbed, conditions can be 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 one apoprotein by chemical nature. They can conditionally be classified as LDL, which contain about 95% of apoprotein-B. All the rest are secondary lipoproteins, which are associated complexes of apoproteins.

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)