Lipids - varied in chemical structure 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, together with proteins and carbohydrates, the main structural component of living cells. 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 breakdown of which releases a large number of energy...
others are the most important structural components cell membranes (free cholesterol and phospholipids). Lipids are involved in the processes of thermoregulation, protection of vital important organs(for example, kidneys) from mechanical stress (trauma), protein loss, in creating elasticity skin, protecting them from excessive moisture removal.
Some of the lipids are biologically active substances that have the properties of modulators of hormonal effects (prostaglandins) and vitamins (polyunsaturated fatty acids). Moreover, lipids promote the absorption of fat-soluble vitamins A, D, E, K; act as antioxidants (vitamins A, E), which largely regulate 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 significance of determining 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 a physiological phenomenon can be observed 1.5 hours after a meal. 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 in a number of pathological conditions. So, in patients 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 is a 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).
Pathophysiological mechanisms, causing shifts 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 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 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.
A high risk of developing coronary atherosclerosis in people aged 30-39 and over 40 years old occurs when cholesterol levels exceed 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 connection between hypercholesterolemia and coronary atherosclerosis, the incidence of coronary artery disease and myocardial infarction.
The highest level of cholesterol is observed with genetic disorders in lipid metabolism: familial homo- and 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 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 failure 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.
Determination of the fractional composition of cholesterol in blood plasma and its individual lipids (primarily HDL) has acquired great diagnostic significance 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 main components of HDL - apo - Al, constantly synthesized in the liver.
A nonspecific activator of the plasma cholesterol esterification system is albumin, also produced by hepatocytes. 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 It also decreases in chronic alcoholism. A sharp decrease in the severity of the cholesterol esterification process indicates insufficiency of liver function.
Clinical and diagnostic value of concentration studies
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. Depending 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. For this purpose, lipid thin layer chromatography methods have been widely used in recent years.
Composition and properties of blood plasma lipoproteins
Almost all plasma lipids are bound to proteins, which makes them highly soluble 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, lipids are peculiar globules, inside of which there is a fat droplet, 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.
Physical Features 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 , i.e. their nature.
The largest particles, consisting of 98% lipids and a very small (about 2%) proportion of protein, are chylomicrons (CM). 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 serum lipoproteins
| 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 total 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 total 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 refers to 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 the outer membrane of the endothelial, smooth muscle and any other cell, favorable conditions are created for the transfer of excess free cholesterol to HDL.
However, the latter remains in the surface HDL monolayer only for a very short time, since it undergoes esterification with the participation of the LCAT enzyme. 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.
If the balance is disturbed between the processes of the influx of lipids (cholesterol) into the vascular wall and their outflow from it, conditions can be created for the formation of lipoidosis, the most known manifestation 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 can conditionally 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 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 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
For the differential diagnosis of IHD, another indicator is used - cholesterol atherogenic coefficient . It can be calculated using the formula: LDL cholesterol + VLDL cholesterol / HDL cholesterol.
More often used in clinical practice Klimov coefficient, which is calculated as follows: Total cholesterol – HDL cholesterol / HDL cholesterol. In healthy people, the Klimov coefficient Not exceeds "3" The higher this coefficient, the higher the risk of developing IHD.
System “lipid peroxidation – antioxidant protection of the body”
In recent years, interest in the clinical aspects of studying the process of free radical lipid peroxidation has increased immeasurably. This is largely due to the fact that a defect in this metabolic link can significantly reduce the body’s resistance to the effects of unfavorable factors of the external and internal environment, as well as create prerequisites for the formation, accelerated development and aggravation of the severity of various diseases of vital organs: lungs, heart , liver, kidneys, etc. Characteristic feature This so-called free radical pathology involves damage to membranes, which is why it is also called membrane pathology.
The deterioration of the environmental situation noted in recent years, associated with prolonged exposure of people to ionizing radiation, progressive pollution of the air with dust particles, exhaust gases and other toxic substances, as well as soil and water with nitrites and nitrates, chemicalization of various industries, smoking, and alcohol abuse have led to to the fact that, under the influence of radioactive contamination and foreign substances, very reactive substances began to form in large quantities, significantly disrupting the course of metabolic processes. What all these substances have in common is the presence of unpaired electrons in their molecules, which makes it possible to classify these intermediates as so-called free radicals (FR).
Free radicals are particles that differ from ordinary ones in that in the electron layer of one of their atoms in the outer orbital there are not two electrons mutually holding each other, making this orbital filled, but only one.
When the outer orbital of an atom or molecule is filled with two electrons, a particle of substance acquires more or less pronounced chemical stability, whereas if there is only one electron in the orbital, due to the influence it exerts - the uncompensated magnetic moment and the high mobility of the electron within the molecule - the chemical activity of the substance increases sharply.
CPs can be formed by the abstraction of a hydrogen atom (ion) from a molecule, as well as the addition (incomplete reduction) or donation (incomplete oxidation) of one of the electrons. It follows that free radicals can be represented either by electrically neutral particles or by particles carrying a negative or positive charge.
One of the most widespread free radicals in the body is the product of incomplete reduction of an oxygen molecule - superoxide anion radical (O 2 -). It is constantly formed with the participation of special enzyme systems in the cells of many pathogenic bacteria, blood leukocytes, macrophages, alveolocytes, cells of the intestinal mucosa, which have an enzyme system that produces this superoxide anion-oxygen radical. Mitochondria make a major contribution to O2 synthesis as a result of the “draining” of some electrons from the mitochondrial chain and transferring them directly to molecular oxygen. This process is significantly activated under conditions of hyperoxia (hyperbaric oxygenation), which explains the toxic effects of oxygen.
Two installed lipid peroxidation pathways:
1) non-enzymatic, ascorbate dependent, activated by metal ions of variable valency; since during the oxidation process Fe ++ turns into Fe +++, its continuation requires the reduction (with the participation of ascorbic acid) of oxide iron into ferrous iron;
2) enzymatic, NADPH-dependent, carried out with the participation of NADP H-dependent microsomal dioxygenase, generating O — 2 .
Lipid peroxidation occurs through the first pathway in all membranes, while through the second, it occurs only in the endoplasmic reticulum. To date, other special enzymes are known (cytochrome P-450, lipoxygenases, xanthine oxidases) that form free radicals and activate lipid peroxidation in microsomes (microsomal oxidation), other cell organelles with the participation of NADPH, pyrophosphate and ferrous iron as cofactors. With a hypoxia-induced decrease in pO2 in tissues, xanthine dehydrogenase is converted into xanthine oxidase. In parallel with this process, another is activated - the conversion of ATP into hypoxanthine and xanthine. When xanthine oxidase acts on xanthine, it forms superoxide oxygen radical anions. This process is observed not only during hypoxia, but also during inflammation, accompanied by stimulation of phagocytosis and activation of the hexose monophosphate shunt in leukocytes.
Antioxidant systems
The described process would develop uncontrollably if the cellular elements of the tissues did not contain substances (enzymes and non-enzymes) that counteract its progress. They became known as antioxidants.
Non-enzymatic free radical oxidation inhibitors are natural antioxidants - alpha-tocopherol, steroid hormones, thyroxine, phospholipids, cholesterol, retinol, ascorbic acid.
Basic natural antioxidant alpha-tocopherol is found not only in plasma, but also in red blood cells. It is believed that molecules alpha tocopherol, are embedded in the lipid layer of the erythrocyte membrane (as well as all other cell membranes of the body), protect unsaturated fatty acids of phospholipids from peroxidation. The preservation of the structure of cell membranes largely determines their functional activity.
The most common antioxidant is alpha tocopherol (vitamin E), containing in plasma and plasmatic cell membranes, retinol (vitamin A), ascorbic acid, some enzymes, for example superoxide dismutase (SOD) red blood cells and other tissues, ceruloplasmin(destroying superoxide anion radicals of oxygen in blood plasma), glutathione peroxidase, glutathione reductase, catalase etc., influencing the content of LPO products.
With a sufficiently high content of alpha-tocopherol in the body, only a small amount of lipid peroxidation products are formed, which are involved in the regulation of many physiological processes, including: cell division, ion transport, renewal of cell membranes, in the biosynthesis of hormones, prostaglandins, and in the implementation of oxidative phosphorylation. A decrease in the content of this antioxidant in tissues (causing a weakening of the body's antioxidant defense) leads to the fact that the products of lipid peroxidation begin to produce a pathological effect instead of a physiological one.
Pathological conditions, characterized increased formation of free radicals and activation of lipid peroxidation, may represent independent diseases, largely similar in pathobiochemical and clinical manifestations ( vitamin deficiency E, radiation damage, some poisonings chemicals ). At the same time, the initiation of free radical oxidation of lipids plays an important role in formation of various somatic diseases associated with damage to internal organs.
LPO products formed in excess cause disruption not only of lipid interactions in biomembranes, but also of their protein component - due to binding to amine groups, which leads to disruption of the protein-lipid relationship. As a result, the accessibility of the hydrophobic layer of the membrane for phospholipases and proteolytic enzymes increases. This enhances the processes of proteolysis and, in particular, the breakdown of lipoprotein proteins (phospholipids).
Free radical oxidation causes changes in elastic fibers, initiates fibroplastic processes and aging collagen. In this case, the most vulnerable are the membranes of erythrocyte cells and arterial endothelium, since they, having a relatively high content of easily oxidized phospholipids, come into contact with a relatively high concentration of oxygen. Destruction of the elastic layer of the parenchyma of the liver, kidneys, lungs and blood vessels entails fibrosis, including pneumofibrosis(for inflammatory lung diseases), atherosclerosis and calcification.
The pathogenetic role is beyond doubt activation of sex in the formation of disorders in the body under chronic stress.
A close correlation has been found between the accumulation of lipid peroxidation products in the tissues of vital organs, plasma and erythrocytes, which makes it possible to use blood to judge the intensity of free radical oxidation of lipids in other tissues.
The pathogenetic role of lipid peroxidation in the formation of atherosclerosis and coronary disease heart, diabetes mellitus, malignant neoplasms, hepatitis, cholecystitis, burn disease, pulmonary tuberculosis, bronchitis, nonspecific pneumonia.
The establishment of LPO activation in a number of diseases of internal organs was the basis for use with therapeutic purpose antioxidants of various natures.
Their use gives a positive effect in chronic ischemic heart disease, tuberculosis (also causing the elimination adverse reactions on antibacterial drugs: streptomycin, etc.), many other diseases, as well as chemotherapy for malignant tumors.
Antioxidants are increasingly used to prevent the consequences of exposure to certain toxic substances, weaken the “spring weakness” syndrome (believed to be caused by intensified lipid peroxidation), prevent and treat atherosclerosis, and many other diseases.
Apples have a relatively high alpha-tocopherol content, wheat germ, wheat flour, potatoes, beans.
To diagnose pathological conditions and evaluate the effectiveness of treatment, it is customary to determine the content of primary (diene conjugates), secondary (malondialdehyde) and final (Schiff bases) LPO products in blood plasma and erythrocytes. In some cases, the activity of antioxidant enzymes is studied: SOD, ceruloplasmin, glutathione reductase, glutathione peroxidase and catalase. Integral test for assessing gender is determination of the permeability of erythrocyte membranes or the osmotic resistance of erythrocytes.
It should be noted that pathological conditions characterized by increased formation of free radicals and activation of lipid peroxidation can be:
1) an independent disease with a characteristic clinical picture, for example, vitamin E deficiency, radiation injury, some chemical poisonings;
2) somatic diseases associated with damage to internal organs. These include primarily: chronic ischemic heart disease, diabetes mellitus, malignant neoplasms, inflammatory diseases lungs (tuberculosis, nonspecific inflammatory processes in the lungs), liver diseases, cholecystitis, burn disease, gastric and duodenal ulcers.
It should be borne in mind that the use of a number of well-known drugs (streptomycin, tubazide, etc.) in the process of chemotherapy for pulmonary tuberculosis and other diseases (streptomycin, tubazide, etc.) can itself cause activation of lipid peroxidation, and, consequently, aggravation of the severity of the disease.
Hyperlipidemia (hyperlipemia) - an increase in the concentration of total plasma lipids as a physiological phenomenon can be observed 1-4 hours after a meal. 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 in a number of pathological conditions:
Nephrotic syndrome, lipoid nephrosis, acute and chronic nephritis;
Biliary cirrhosis of the liver, acute hepatitis;
Obesity - atherosclerosis;
Hypothyroidism;
Pancreatitis, etc.
The study of cholesterol (CH) levels reflects only the pathology of lipid metabolism in the body. Hypercholesterolemia is a documented risk factor for coronary atherosclerosis. CS is an essential component of the membrane of all cells, special physicochemical characteristics CS crystals and the conformation of its molecules contribute to the ordering and mobility of phospholipids in membranes when temperature changes, which allows the membrane to be in an intermediate phase state (“gel - liquid crystal”) and maintain physiological functions. CS is used as a precursor in the biosynthesis of steroid hormones (gluco- and mineralocorticoids, sex hormones), vitamin D 3, and bile acids. Conventionally, we can distinguish 3 pools of cholesterol:
A - quickly exchanging (30 g);
B – slowly exchanging (50 g);
B – very slowly exchanging (60 g).
Endogenous cholesterol is synthesized in significant quantities in the liver (80%). Exogenous cholesterol enters the body as part of animal products. Transport of cholesterol from the liver to extrahepatic tissues is carried out
LDL. The removal of cholesterol from the liver from extrahepatic tissues into the liver is produced by mature forms of HDL (50% - LDL, 25% HDL, 17% VLDL, 5% -CM).
Hyperlipoproteinemia and hypercholesterolemia (Fredrickson classification):
Type 1 – hyperchylomicronemia;
type 2 - a - hyper-β-lipoproteinemia, b - hyper-β and hyperpre-β-lipoproteinemia;
type 3 – dys-β-lipoproteinemia;
type 4 – hyper-pre-β-lipoproteinemia;
Type 5 – hyper-pre-β-lipoproteinemia and hyperchylomicronemia.
The most atherogenic are types 2 and 3.
Phospholipids are a group of lipids containing, in addition to phosphoric acid (an essential component), alcohol (usually glycerol), fatty acid residues and nitrogenous bases. In clinical and laboratory practice, there is a method for determining the level of total phospholipids, the level of which increases in patients with primary and secondary hyperlipoproteinemia IIa and IIb. A decrease occurs in a number of diseases:
Nutritional dystrophy;
Fatty liver degeneration,
Portal cirrhosis;
Progression of atherosclerosis;
Hyperthyroidism, etc.
Lipid peroxidation (LPO) is a free radical process, the initiation of which occurs with the formation of reactive oxygen species - superoxide ion O 2 . ; hydroxyl radical HO . ; hydroperoxide radical HO 2 . ; singlet oxygen O 2 ; hypochlorite ion ClO - . The main substrates of LPO are polyunsaturated fatty acids found in the structure of membrane phospholipids. The strongest catalyst is iron metal ions. LPO is a physiological process that is important for the body, as it regulates membrane permeability, affects cell division and growth, begins phagosynthesis, and is a pathway for the biosynthesis of certain biological substances(prostaglandins, thromboxanes). The level of lipid peroxidation is controlled by the antioxidant system (ascorbic acid, uric acid, β-carotene, etc.). Loss of balance between the two systems leads to the death of cells and cellular structures.
For diagnostic purposes, it is customary to determine the content of lipid peroxidation products (diene conjugates, malondialdehyde, Schiff bases) and the concentration of the main natural antioxidant - alpha-tocopherol in plasma and red blood cells with the calculation of the MDA/TF coefficient. An integral test for assessing LPO is determining the permeability of erythrocyte membranes.
2. Pigment exchange a set of complex transformations of various colored substances in the human and animal body.
The most well-known blood pigment is hemoglobin (a chromoprotein that consists of the protein part of globin and a prosthetic group represented by 4 hemes, each heme consists of 4 pyrrole nuclei, which are interconnected by methine bridges, in the center there is an iron ion with an oxidation state of 2 +) . Average term The life of an erythrocyte is 100-110 days. At the end of this period, destruction and destruction of hemoglobin occurs. The decay process begins already in the vascular bed and ends in the cellular elements of the system of phagocytic mononuclear cells (Kupffer cells of the liver, connective tissue histiocytes, bone marrow plasma cells). Hemoglobin in the vascular bed binds to plasma haptoglobin and is retained in the vascular bed without passing through the renal filter. Due to the trypsin-like action of the beta chain of haptoglobin and the conformational changes caused by its influence in the porphyrin ring of the heme, conditions are created for easier destruction of hemoglobin in the cellular elements of the phagocytic mononuclear system. The resulting high-molecular green pigment verdoglobin(synonyms: verdohemoglobin, choleglobin, pseudohemoglobin) is a complex consisting of globin, a broken porphyrin ring system and ferric iron. Further transformations lead to the loss of iron and globin by verdoglobin, as a result of which the porphyrin ring unfolds into a chain and a low molecular weight green bile pigment is formed - biliverdin. Almost all of it is enzymatically restored into the most important red-yellow pigment of bile - bilirubin, which is a common component of blood plasma. It undergoes dissociation on the surface of the plasma membrane of the hepatocyte. In this case, the released bilirubin forms a temporary associate with the lipids of the plasma membrane and moves through it due to the activity of certain enzyme systems. Further passage of free bilirubin into the cell occurs with the participation of two carrier proteins in this process: ligandin (it transports the main amount of bilirubin) and protein Z.
Ligandin and protein Z are also found in the kidneys and intestines, therefore, in case of insufficient liver function, they are free to compensate for the weakening of detoxification processes in this organ. Both are quite soluble in water, but lack the ability to move through the lipid layer of the membrane. By binding bilirubin to glucuronic acid, the inherent toxicity of free bilirubin is largely lost. Hydrophobic, lipophilic free bilirubin, easily dissolving in membrane lipids and thereby penetrating into mitochondria, uncouples respiration and oxidative phosphorylation in them, disrupts protein synthesis, the flow of potassium ions through the membrane of cells and organelles. This negatively affects the state of the central nervous system, causing a number of characteristic neurological symptoms in patients.
Bilirubin glucuronides (or bound, conjugated bilirubin), unlike free bilirubin, immediately react with the diazo reagent (“direct” bilirubin). It should be borne in mind that in the blood plasma itself, bilirubin that is not conjugated with glucuronic acid can either be associated with albumin or not. The last fraction (bilirubin not associated with albumin, lipids, or other blood components) is the most toxic.
Bilirubin glucuronides, thanks to membrane enzyme systems, actively move through them (against the concentration gradient) into the bile ducts, being released along with bile into the intestinal lumen. In it, under the influence of enzymes produced by intestinal microflora, the glucuronide bond is broken. The released free bilirubin is reduced to form first mesobilirubin and then mesobilinogen (urobilinogen) in the small intestine. Normally, a certain part of mesobilinogen, absorbed in the small intestine and in the upper part of the colon, enters the liver through the portal vein system, where it is almost completely destroyed (by oxidation), turning into dipyrrolic compounds - propent-diopent and mesobileucane.
Mesobilinogen (urobilinogen) does not enter the general circulation. Part of it, together with the products of destruction, is again sent into the intestinal lumen as part of bile (enterohepotic circulation). However, even with the most minor changes in the liver, its barrier function is largely “removed” and mesobilinogen enters first into the general blood circulation and then into the urine. The bulk of it is sent from the small intestine to the large intestine, where, under the influence of anaerobic microflora (Escherichia coli and other bacteria), it undergoes further reduction with the formation of stercobilinogen. The resulting stercobilinogen (daily amount 100-200 mg) is almost completely excreted in the feces. In air, it oxidizes and turns into stercobilin, which is one of the pigments of feces. Small part Stercobilinogen is absorbed through the mucous membrane of the large intestine into the inferior vena cava system, delivered in the blood to the kidneys and excreted in the urine.
Thus, in the urine of a healthy person, mesobilinogen (urobilinogen) is absent, but it contains a certain amount of stercobilin (which is often incorrectly called “urobilin”)
To determine the content of bilirubin in blood serum (plasma), mainly chemical and physicochemical research methods are used, among which are colorimetric, spectrophotometric (manual and automated), chromatographic, fluorimetric and some others.
One of the important subjective signs of a disorder of pigment metabolism is the appearance of jaundice, which is usually noted when the level of bilirubin in the blood is 27-34 µmol/l or more. The causes of hyperbilirubinemia can be: 1) increased hemolysis of red blood cells (more than 80% of total bilirubin is represented by unconjugated pigment); 2) impaired liver cell function and 3) delayed bile outflow (hyperbilirubinemia is of hepatic origin if more than 80% of total bilirubin is conjugated bilirubin). In the first case, they talk about the so-called hemolytic jaundice, in the second – about parenchymal jaundice (can be caused by hereditary defects in the processes of transport of bilirubin and its glucuronidation), in the third – about mechanical (or obstructive, congestive) jaundice.
With parenchymal form of jaundice Destructive-dystrophic changes are observed in the parenchymal cells of the liver and infiltrative ones in the stroma, leading to increased pressure in the bile ducts. Stagnation of bilirubin in the liver is also facilitated by a sharp weakening of metabolic processes in affected hepatocytes, which lose the ability to normally perform various biochemical and physiological processes, in particular, transfer bound bilirubin from cells into bile against a concentration gradient. An increase in the concentration of conjugated bilirubin in the blood leads to its appearance in the urine.
The most “subtle” sign of liver damage in hepatitis is the appearance mesobilinogen(urobilinogen) in the urine.
With parenchymal jaundice, the concentration of bound (conjugated) bilirubin in the blood increases mainly. The content of free bilirubin increases, but to a lesser extent.
The pathogenesis of obstructive jaundice is based on the cessation of bile flow into the intestine, which leads to the disappearance of stercobilinogen from the urine. With congestive jaundice, the content of conjugated bilirubin in the blood increases mainly. Extrahepatic cholestatic jaundice is accompanied by a triad of clinical signs: discolored stool, dark urine and itchy skin. Intrahepatic cholestasis is clinically manifested by skin itching and jaundice. At laboratory research hyperbilirubinemia (due to associated), bilirubinuria, increased alkaline phosphatase with normal values of transaminases in the blood serum are noted.
Hemolytic jaundice are caused by hemolysis of red blood cells and, as a consequence, increased formation of bilirubin. An increase in free bilirubin is one of the main signs of hemolytic jaundice.
In clinical practice, congenital and acquired functional hyperbilirubinemia is distinguished, caused by a violation of the elimination of bilirubin from the body (the presence of defects in enzyme and other systems for the transfer of bilirubin through cell membranes and its glucuronidation in them). Gilbert's syndrome is a hereditary benign chronic disease that occurs with moderate non-hemolytic unconjugated hyperbilirubinemia. Post-hepatitis hyperbilirubinemia Kalka - acquired enzyme defect leading to an increase in the level of free bilirubin in the blood, congenital familial non-hemolytic jaundice of Crigler - Nayjar (absence of glucuronyltransferase in hepatocytes), jaundice with congenital hypothyroidism (thyroxine stimulates the enzyme glucuronyltransferase system), physiological jaundice of newborns, drug jaundice, etc. .
Disturbances in pigment metabolism can be caused by changes not only in the processes of heme decomposition, but also in the formation of its precursors - porphyrins (cyclic organic compounds based on a porphin ring consisting of 4 pyrroles connected by methine bridges). Porphyrias are a group of hereditary diseases accompanied by a genetic deficiency in the activity of enzymes involved in heme biosynthesis, in which an increase in the content of porphyrins or their precursors is detected in the body, which causes a number of clinical signs (excessive formation of metabolic products, causes the development of neurological symptoms and (or) increased skin photosensitivity).
The most widely used methods for the determination of bilirubin are based on its interaction with a diazoreagent (Ehrlich's reagent). The Jendrassik-Grof method has become widespread. In this method, a mixture of caffeine and sodium benzoate in acetate buffer is used as a “liberator” of bilirubin. The enzymatic determination of bilirubin is based on its oxidation by bilirubin oxidase. It is possible to determine unconjugated bilirubin by other methods of enzymatic oxidation.
Currently, the determination of bilirubin using “dry chemistry” methods is becoming increasingly widespread, especially in rapid diagnostics.
Vitamins.
Vitamins are essential low-molecular substances that enter the body with food from the outside and are involved in the regulation of biochemical processes at the enzyme level.
Similarities and differences between vitamins and hormones.
Similarities– regulate metabolism in the human body through enzymes:
· Vitamins are part of enzymes and are coenzymes or cofactors;
· Hormones or regulate the activity of existing enzymes in the cell, or are inducers or repressors in the biosynthesis of necessary enzymes.
Difference:
· Vitamins– low-molecular organic compounds, exogenous factors regulating metabolism and come from food from the outside.
· Hormones– high-molecular organic compounds, endogenous factors synthesized in the endocrine glands of the body in response to changes in the external or internal environment of the human body, and also regulate metabolism.
Vitamins are classified into:
1. Fat soluble: A, D, E, K, A.
2. Water-soluble: group B, PP, H, C, THFA (tetrahydrofolic acid), pantothenic acid (B 3), P (rutin).
Vitamin A (retinol, antixerophthalmic) – the chemical structure is represented by a β-ionone ring and 2 isoprene residues; The body's need is 2.5-30 mg per day.
The earliest and most specific sign of hypovitaminosis A is hemeralopia (night blindness) - impaired twilight vision. It occurs due to a lack of visual pigment - rhodopsin. Rhodopsin contains retinal (vitamin A aldehyde) as an active group - located in the retinal rods. These cells (rods) perceive low-intensity light signals.
Rhodopsin = opsin (protein) + cis-retinal.
When rhodopsin is excited by light, cis-retinal, as a result of enzymatic rearrangements inside the molecule, transforms into all-trans-retinal (in the light). This leads to a conformational rearrangement of the entire rhodopsin molecule. Rhodopsin dissociates into opsin and trans-retinal, which is a trigger that excites in the endings optic nerve an impulse that is then transmitted to the brain.
In the dark, as a result of enzymatic reactions, trans-retinal is converted back into cis-retinal and, combining with opsin, forms rhodopsin.
Vitamin A also affects the processes of growth and development of the integumentary epithelium. Therefore, with vitamin deficiency, damage to the skin, mucous membranes and eyes is observed, which manifests itself in pathological keratinization of the skin and mucous membranes. Patients develop xerophthalmia - dryness of the cornea of the eye, as the lacrimal canal becomes blocked as a result of keratinization of the epithelium. Since the eye ceases to be washed with tears, which have a bactericidal effect, conjunctivitis, ulceration and softening of the cornea - keratomalacia - develop. With vitamin A deficiency there may also be damage to the gastrointestinal mucosa, respiratory and genitourinary tract. The resistance of all tissues to infections is impaired. With the development of vitamin deficiency in childhood, growth retardation occurs.
Currently, the participation of vitamin A in protecting cell membranes from oxidants has been shown - that is, vitamin A has an antioxidant function.
For the quantitative determination of total lipids in blood serum, the colorimetric method with a phosphovanillin reagent is most often used. Common lipids react after hydrolysis with sulfuric acid with a phosphovanillin reagent to form a red color. The color intensity is proportional to the content of total lipids in the blood serum.
1. Add reagents into three test tubes according to the following scheme:
2. Mix the contents of the test tubes and leave in the dark for 40-60 minutes. (the color of the solution changes from yellow to pink).
3. Mix again and measure the optical density at 500-560 nm (green filter) against a blind sample in a cuvette with a layer thickness of 5 mm.
4. Calculate the amount of total lipids using the formula:
where D 1 is the extinction of the experimental sample in the cuvette;
D 2 – extinction of the calibration solution of lipids in the cuvette;
X is the concentration of total lipids in the standard solution.
Define the concept of “total lipids”. Compare the value you obtained with the normal values. What biochemical processes can be judged by this indicator?
Experiment 4. Determination of the content of b- and pre-b-lipoproteins in blood serum.
2. Set of pipettes.
3. Glass rod.
5. Cuvettes, 0.5 cm.
Reagents. 1. Blood serum.
2. Calcium chloride, 0.025 M solution.
3. Heparin, 1% solution.
4. Distilled water.
1. Pour 2 ml of 0.025 M calcium chloride into a test tube and add 0.2 ml of blood serum.
2. Mix and measure the optical density of the sample (D 1) on FEC-e at a wavelength of 630-690 nm (red filter) in a cuvette with a layer thickness of 0.5 cm against distilled water. Record the optical density D 1 value.
3. Then add 0.04 ml of a 1% heparin solution (1000 units in 1 ml) to the cuvette and measure the optical density D2 again exactly after 4 minutes.
The difference in values (D 2 – D 1) corresponds to the optical density due to the sediment of b-lipoproteins.
Calculate the content of b- and pre-b-lipoproteins using the formula:
where 12 is the coefficient for conversion to g/l.
Indicate the place of biosynthesis of b-lipoproteins. What function do they perform in the human and animal body? Compare the value you obtained with the normal values. In what cases are deviations from normal values observed?
Lesson No. 16. “Lipid metabolism (part 2)”
Purpose of the lesson: study the processes of catabolism and anabolism of fatty acids.
QUESTIONS FOR THE TEST:
1. Biochemical mechanism of fatty acid oxidation.
2. Metabolism of ketone bodies: formation, biochemical purpose. What factors predispose to the development of ketosis in animals?
3. Biochemical mechanism of fatty acid synthesis.
4. Biosynthesis of triacylglycerols. Biochemical role of this process.
5. Biosynthesis of phospholipids. Biochemical role of this process.
Date of completion ________ Point ____ Teacher's signature ____________
Experimental work.
Experiment 1. Express method for determining ketone bodies in urine, milk, blood serum (Lestrade test).
Devices. 1. Rack with test tubes.
2. Set of pipettes.
3. Glass rod.
4. Filter paper.
Reagents. 1. Reagent powder.
3. Blood serum.
4. Milk.
1. Place a small amount (0.1-0.2 g) of reagent powder on the filter paper at the tip of the scalpel.
2. Transfer a few drops of blood serum to the reagent powder.
The minimum level of ketone bodies in the blood that gives positive reaction, equal to 10 mg/100 ml (10 mg%). The rate of color development and its intensity are proportional to the concentration of ketone bodies in the test sample: if the violet color appears immediately - the content is 50-80 mg% or more; if it appears after 1 minute, the sample contains 30-50 mg%; the development of a faint color after 3 minutes indicates the presence of 10-30 mg% ketone bodies.
It should be remembered that the test is more than 3 times more sensitive when determining acetoacetic acid than acetone. Of all the ketone bodies in human serum, acetoacetic acid is predominant, but in the blood of healthy cows, 70-90% of ketone bodies are b-hydroxybutyric acid, and in milk it accounts for 87-92%.
Draw a conclusion based on the results of your research. Explain why excessive formation of ketone bodies is dangerous in the human and animal body?
They have different densities and are indicators of lipid metabolism. There are various methods for the quantitative determination of 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 in a free state, but as part of protein-lipid complexes: chylomicrons, α-lipoproteins, β-lipoproteins. Lipoproteins can be separated various methods: centrifugation in saline solutions of 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 of heparin and 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 liver diseases, diabetes, glycogenosis, xanthomatosis and obesity, a decrease is observed 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 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, 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. The reaction is caused by the formation of green sulfonic acid cholesterylene.
Reagents: Liebermann-Burkhard 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, 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. The normal content of total cholesterol (free and esterified) in blood serum is 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. In case of violation fat metabolism cholesterol can accumulate in the blood. An increase in cholesterol in the blood (hypercholesterolemia) is observed in atherosclerosis, diabetes mellitus, obstructive jaundice, nephritis, nephrosis (especially lipoid nephrosis), hypothyroidism. A decrease in cholesterol in the blood (hypocholesterolemia) is observed with anemia, fasting, tuberculosis, hyperthyroidism, cancer cachexia, parenchymal jaundice, damage to the central nervous system, febrile states, when administered
Determination of blood lipid profile indicators is necessary for the diagnosis, treatment and prevention of cardiovascular diseases. The most important mechanism for the development of such a pathology is the formation of atherosclerotic plaques on the inner wall of blood vessels. Plaques are accumulations of fat-containing compounds (cholesterol and triglycerides) and fibrin. The higher the concentration of lipids in the blood, the more likely the occurrence of atherosclerosis. Therefore, it is necessary to systematically take a blood test for lipids (lipidogram), this will help to promptly identify deviations in fat metabolism from the norm.
Lipidogram - a study that determines the level of lipids of various fractions
Atherosclerosis is dangerous due to the high probability of complications - stroke, myocardial infarction, gangrene lower limbs. These diseases often end in disability of the patient, and in some cases even fatal.
The role of lipids
Functions of lipids:
- Structural. Glycolipids, phospholipids, cholesterol are the most important components of cell membranes.
- Thermal insulation and protective. Excess fat is deposited in subcutaneous fat, reducing heat loss and protecting internal organs. If necessary, the lipid supply is used by the body to obtain energy and simple compounds.
- Regulatory. Cholesterol is necessary for the synthesis of adrenal steroid hormones, sex hormones, vitamin D, bile acids, is part of the myelin sheaths of the brain, and is needed for the normal functioning of serotonin receptors.
Lipidogram
A lipidogram can be prescribed by a doctor both if an existing pathology is suspected, and for preventive purposes, for example, during a medical examination. It includes several indicators that allow you to fully assess the state of fat metabolism in the body.
Lipid profile indicators:
- Total cholesterol (TC). This the most important indicator The lipid spectrum of the blood includes free cholesterol, as well as cholesterol contained in lipoproteins and associated with fatty acids. A significant portion of cholesterol is synthesized by the liver, intestines, and gonads; only 1/5 of the TC comes from food. With normally functioning mechanisms of lipid metabolism, a slight deficiency or excess of cholesterol supplied from food is compensated by an increase or decrease in its synthesis in the body. Therefore, hypercholesterolemia is most often caused not by excess cholesterol intake from foods, but by a failure of the fat metabolism process.
- High density lipoproteins (HDL). This indicator has an inverse relationship with the likelihood of developing atherosclerosis - an increased level of HDL is considered an anti-atherogenic factor. HDL transports cholesterol to the liver, where it is utilized. Women have higher HDL levels than men.
- Low density lipoproteins (LDL). LDL carries cholesterol from the liver to tissues, otherwise known as “bad” cholesterol. This is due to the fact that LDL is capable of forming atherosclerotic plaques, narrowing the lumen of blood vessels.
This is what an LDL particle looks like
- Very low density lipoproteins (VLDL). The main function of this group of particles, heterogeneous in size and composition, is the transport of triglycerides from the liver to tissues. A high concentration of VLDL in the blood leads to clouding of the serum (chylosis), and the possibility of the appearance of atherosclerotic plaques also increases, especially in patients with diabetes mellitus and kidney pathologies.
- Triglycerides (TG). Like cholesterol, triglycerides are transported through the bloodstream as part of lipoproteins. Therefore, an increase in the concentration of TG in the blood is always accompanied by an increase in cholesterol levels. Triglycerides are considered the main source of energy for cells.
- Atherogenic coefficient. It allows you to assess the risk of developing vascular pathology and is a kind of summary of the lipid profile. To determine the indicator, you need to know the value of TC and HDL.
Atherogenic coefficient = (TC - HDL)/HDL
Optimal blood lipid profile values
| Floor | Indicator, mmol/l | |||||
| OH | HDL | LDL | VLDL | TG | CA | |
| Male | 3,21 — 6,32 | 0,78 — 1,63 | 1,71 — 4,27 | 0,26 — 1,4 | 0,5 — 2,81 | 2,2 — 3,5 |
| Female | 3,16 — 5,75 | 0,85 — 2,15 | 1,48 — 4,25 | 0,41 — 1,63 | ||
It should be taken into account that the value of the measured indicators may vary depending on the units of measurement and the analysis methodology. Normal values also vary depending on the age of the patient; the above figures are averaged for individuals 20 - 30 years old. The level of cholesterol and LDL in men after 30 years tends to increase. In women, indicators increase sharply with the onset of menopause, this is due to the cessation of the antiatherogenic activity of the ovaries. The interpretation of the lipid profile must be carried out by a specialist, taking into account individual characteristics person.
A study of blood lipid levels can be prescribed by a doctor to diagnose dyslipidemia, assess the likelihood of developing atherosclerosis, in some chronic diseases (diabetes mellitus, kidney and liver diseases, thyroid gland), and also as a screening study for early detection persons with lipid profile deviations from the norm.
The doctor gives the patient a referral for a lipid profile
Preparing for the study
Lipid profile values can fluctuate not only depending on the gender and age of the subject, but also on the impact on the body of various external and internal factors. To minimize the likelihood of an unreliable result, you must adhere to several rules:
- You should donate blood strictly in the morning on an empty stomach; in the evening of the previous day, a light dietary dinner is recommended.
- Do not smoke or drink alcohol the night before the test.
- 2-3 days before donating blood, avoid stressful situations and intense physical activity.
- Stop using all medicines and dietary supplements, except for vital ones.
Methodology
There are several methods laboratory evaluation lipid profile. IN medical laboratories analysis can be carried out manually or using automatic analyzers. The advantage of an automated measurement system is the minimal risk of erroneous results, speed of analysis, and high accuracy of the study.
Serum is required for analysis. venous blood patient. Blood is drawn into a vacuum tube using a syringe or vacutainer. To avoid clot formation, the blood tube should be inverted several times and then centrifuged to obtain serum. The sample can be stored in the refrigerator for 5 days.
Taking blood for lipid profile
Nowadays, blood lipids can be measured without leaving home. To do this, you need to purchase a portable biochemical analyzer that allows you to assess the level of total cholesterol in the blood or several indicators at once in a matter of minutes. For the test, a drop of capillary blood is needed; it is applied to the test strip. Test strip is saturated special composition, for each indicator it is different. The results are read automatically after inserting the strip into the device. Thanks to the small size of the analyzer and the ability to operate on batteries, it is convenient to use at home and take with you on a trip. Therefore, persons with a predisposition to cardiovascular diseases It is recommended to have it at home.
Interpretation of results
The most ideal result of the analysis for the patient will be a laboratory conclusion that there are no deviations from the norm. In this case, a person does not have to worry about the state of his circulatory system - the risk of atherosclerosis is practically absent.
Unfortunately, this is not always the case. Sometimes the doctor, after reviewing the laboratory data, makes a conclusion about the presence of hypercholesterolemia. What it is? Hypercholesterolemia is an increase in the concentration of total cholesterol in the blood above normal values, and there is a high risk of developing atherosclerosis and related diseases. This condition may be due to a number of reasons:
- Heredity. Science knows cases of familial hypercholesterolemia (FH), in such a situation the defective gene responsible for lipid metabolism is inherited. Patients experience constantly elevated levels of TC and LDL; the disease is especially severe in the homozygous form of FH. Such patients have an early onset of coronary artery disease (at the age of 5-10 years); in the absence of proper treatment, the prognosis is unfavorable and in most cases ends in death before reaching 30 years of age.
- Chronic diseases. Elevated cholesterol levels are observed in diabetes mellitus, hypothyroidism, kidney and liver pathologies, and are caused by lipid metabolism disorders due to these diseases.
For patients suffering from diabetes, it is important to constantly monitor cholesterol levels
- Poor nutrition. Long-term abuse of fast food, fatty, salty foods leads to obesity, and, as a rule, there is a deviation in lipid levels from the norm.
- Bad habits. Alcoholism and smoking lead to disruptions in the mechanism of fat metabolism, as a result of which the lipid profile increases.
With hypercholesterolemia, it is necessary to adhere to a diet with limited fat and salt, but in no case should you completely abandon all foods rich in cholesterol. Only mayonnaise, fast food and all products containing trans fats should be excluded from the diet. But eggs, cheese, meat, sour cream must be present on the table, you just need to choose products with a lower percentage of fat content. Also important in the diet is the presence of greens, vegetables, cereals, nuts, and seafood. The vitamins and minerals they contain perfectly help stabilize lipid metabolism.
An important condition for normalizing cholesterol is also giving up bad habits. Constant physical activity is also beneficial for the body.
In case if healthy image life in combination with diet did not lead to a decrease in cholesterol, it is necessary to prescribe appropriate drug treatment.
Drug treatment of hypercholesterolemia includes the prescription of statins
Sometimes specialists are faced with a decrease in cholesterol levels - hypocholesterolemia. Most often, this condition is caused by insufficient intake of cholesterol from food. Fat deficiency is especially dangerous for children; in such a situation, there will be a lag in physical and mental development; cholesterol is vital for a growing body. In adults, hypocholesteremia leads to disorders emotional state due to malfunctions of the nervous system, problems with reproductive function, decreased immunity, etc.
Changes in the blood lipid profile inevitably affect the functioning of the entire body, so it is important to systematically monitor fat metabolism indicators for timely treatment and prevention.
