They are micellar structures that differ in molecular weight, the percentage of individual lipid components, the ratio of proteins and lipids. A relatively constant level of lipoproteins circulating in the blood is maintained by the processes of synthesis and secretion of lipid and apoprotein components, active transport of lipids between lipoprotein particles and the presence of a pool of free blood apoproteins, specific transport of plasma proteins, changes in the composition of lipoproteins as a result of processes activated by heparin-dependent lipoprotein lipase (EC 3.1. 1.34), hepatic triacylglycerol lipase (EC 3.1.1.3.), phosphatitdylcholine-cholesterol acyltransferase (EC 2.3.1.43.), removal from circulation by internalization of both lipoproteins and their protein components.
Separate lipoproteins by ultracentrifugation in saline solutions, using their differences in buoyant density. Chylomicrons have a lower floating density, which form a creamy layer on the surface of the serum when stored for a day at a temperature of 0 + 4 ° C, with further saturation of the serum with neutral salts, lipoproteins of very low (VLDL), low (LDL) and high (HDL) can be separated ) density.
Given the different protein content (which is reflected in the total charge of the particles), lipoproteins are separated by electrophoresis in various media (paper, cellulose acetate, polyacrylamide, agar, starch gels). α-lipoproteins (HDL), which contain a larger amount of protein, have the highest mobility in an electric field, followed by β- and preβ-lipoproteins (LDL and VLDL, respectively), and chylomicrons remain near the start line.
| Criteria for assessing lipoproteins | Types of lipoproteins | |||
| HDL | LDL | VLDL | Chylomicrons | |
| Density, g/l | 1063‑1210 | 1010‑1063 | 1010‑930 | 930 |
| Molecular weight, ×10 5 | 1,8‑3,8 | 22,0 | 30,0‑1280,0 | - |
| Size of molecules and particles, nm | 7,0‑10,0 | 10,0‑30,0 | 200,0 | >200 |
| Total proteins, % | 50‑57 | 21‑22 | 5‑12 | 2 |
| Total lipids, % | 43‑50 | 78‑79 | 88‑95 | 98 |
| Major apoproteins | ApoA‑I, C‑I, II, III | Apo B | Apo B, C‑I, II, III | Apo C and B |
| free cholesterol | 2‑3 | 8‑10 | 3‑5 | 2 |
| Esterified cholesterol, % | 19‑20 | 36‑37 | 10‑13 | 4‑5 |
| Phospholipids, % | 22‑24 | 20‑22 | 13‑20 | 4‑7 |
| Total cholesterol / phospholipids | 1,0 | 2,3 | 0,9 | 1,1 |
| Triacylglycerols | 4‑8 | 11‑12 | 50‑60 | 84‑87 |
Normal values
Changes in the spectrum of individual fractions of lipoproteins are not always accompanied by hyperlipidemia, so the greatest clinical and diagnostic value is the identification of types of dyslipoproteinemia, which is carried out according to the principles common with the typing of hyperlipoproteinemia according to Fredrickson et al. (1965, 1971) with the introduction of additional types of hyper-α- and hypo-α-lipoproteinemia and hypoβ-lipoproteinemia:
Type I: Hyperchylomicronemia
Due to genetic lipoprotein lipase defect. As a result, due to a violation of the transformation of chylomicrons into residual (remnant) forms, their apoE receptor endocytosis decreases.
Laboratory indicators:
- a significant increase in the number of chylomicrons;
- normal or slightly elevated levels of preβ-lipoproteins (VLDL);
- a sharp increase in the concentration of TAG.
- CS / TAG ratio< 0,15
Clinically manifested at an early age with xanthomatosis and hepatosplenomegaly as a result of lipid deposition in the skin, liver and spleen. Primary type I hyperlipoproteinemia is rare and manifests at an early age, secondary- accompanies diabetes, lupus erythematosus, nephrosis, hypothyroidism, manifested by obesity.
Type II: Hyper‑β‑lipoproteinemia
1. Subtype IIa (familial hypercholesterolemia):
conditioned structural defect apoB100 receptor and impaired LDL endocytosis. As a result, the elimination of LDL from the bloodstream slows down. In the homozygous form, receptors are absent, in the heterozygous form, their number is halved.
Laboratory indicators:
- high content of β‑lipoproteins (LDL);
- normal content of preβ-lipoproteins (VLDL);
- high cholesterol;
- normal content of triacylglycerols.
2. Subtype IIb:
called functional decrease in activity apoB-100 receptor which develops in violation of the formation of mature forms of LDL. The cause of LDL maturation block is
- apoprotein D deficiency, while HDL and LDL do not interact,
- decreased activity of the enzyme lecithin-cholesterol-acyltransferase,
- apoprotein A-1 defect, which leads to disruption of the functioning of HDL,
- association of the acute phase protein of amyloid A with HDL and, as a result, a violation of the LCAT reaction and the functioning of HDL.
Laboratory indicators:
- high cholesterol;
- moderate increase in triacylglycerols.
Clinically manifested by atherosclerotic disorders. Primary hyper β-lipoproteinemia is more common and is observed already at an early age. In the case of the homozygous form, it ends in death from myocardial infarction at a young age, secondary observed in nephrosis, liver disease, multiple myeloma, macroglobulinemia.
Type III: Dysβ‑lipoproteinemia
or hyperβ‑hyperpreβ‑lipoproteinemia
conditioned apoprotein E defect, responsible for the binding of residual chylomicrons and VLDL to receptors on the hepatocyte. As a result, the extraction of these particles from the blood is reduced.
Laboratory indicators:
- an increase in the concentration of β‑lipoproteins (LDL) and preβ‑lipoproteins (VLDL);
- high levels of cholesterol and triacylglycerols;
- the ratio of cholesterol / TAG = 0.3‑2.0 (often around 1.0).
Clinically manifested by atherosclerosis with coronary disorders, more common in adults. Some patients have flat, tuberculate and eruptive xanthomas. Secondary type III hyperlipoproteinemia occurs in patients with systemic lupus erythematosus and diabetic ketoacidosis.
Type IV. Hyperpreβ‑lipoproteinemia
Caused by inadequately high synthesis of triacylglycerols in the liver as a result of excess glucose intake.
Laboratory indicators:
- increase in VLDL;
- increased levels of triacylglycerides;
- normal or slightly elevated cholesterol levels.
Primary hyperlipoproteinemia type IV leads to the development of obesity and atherosclerosis after 20 years, secondary- observed with overeating, hypothyroidism, type 2 diabetes mellitus, pancreatitis, nephrosis, alcoholism.
Type V: Hyperchylomicronemia and hyperpreβ-lipoproteinemia
Caused by a moderate decrease in the activity of lipoprotein lipase as a result of apoCII protein defect, which leads to the accumulation of chylomicrons and VLDL in the blood.
Laboratory indicators:
- increased levels of chylomicrons;
- increased levels of preβ-lipoproteins (VLDL);
- the content of triglycerols is increased, in some cases sharply;
- cholesterol levels are normal or moderately elevated;
- the ratio of cholesterol / TAG = 0.15‑0.60
Clinically manifested as the first type.
Hyper‑α‑lipoproteinemia.
Laboratory indicators:
- increase in the amount of HDL;
- an increase in the level of α‑cholesterol over 2 mmol / l.
There are cases of familial hyper-α-cholesterolemia and an increase in HDL in the blood during training for prolonged physical exertion.
Alipoproteinemia
1. An‑α‑lipoproteinemia (Tangier disease).
It is caused by a congenital disorder in the synthesis of apoproteins A‑I and A‑II.
Laboratory indicators:
- the absence of normal and the appearance of abnormal HDL;
- reduction in total cholesterol to 0.26 mmol/l or less;
- an increase in the proportion of cholesterol esters.
Clinical manifested by tonsillitis, early developing atherosclerosis and coronary heart disease.
2. An‑β‑lipoproteinemia.
It is caused by a decrease in the synthesis of apoprotein B in the liver.
Laboratory indicators:
- decrease in the number of chylomicrons;
- decrease in the level of VLDL and LDL.
- lowering cholesterol to 0.5‑2.0 mmol/l;
- reduction of triglycerides to 0‑0.2 g/l.
It is clinically manifested by malabsorption of dietary fats, retinitis pigmentosa, acanthosis and ataxic neuropathy.
Hypolipoproteinemia
1. Hypo‑α‑lipoproteinemia is often combined with an increase in VLDL and LDL in the blood. Clinically manifested as II, IV and V types of hyperlipoproteinemia, which increases the risk of atherosclerosis and its complications.
2. Hypo‑β‑lipoproteinemia is expressed in a decrease in LDL in the blood. It is clinically manifested by a violation of the absorption of dietary fats in the intestine.
LCAT-deficiency
It is caused by a genetic deficiency of the enzyme lecithin:cholesterol-acyl-transferase.
Laboratory indicators:
- decrease in the cholesterol esterification coefficient;
- violation of the chemical composition and structure of all classes of lipoproteins.
- the appearance of abnormal lipoprotein X in the LDL fraction.
It is clinically manifested by hypochromic anemia, renal failure, splenomegaly, corneal clouding due to the accumulation of non-esterified cholesterol in the cell membranes of the kidneys, spleen, cornea, and erythrocytes.
Determination of β- and preβ-lipoproteins in blood serum by Burshtein turbidimetric method
Principle
In the presence of CaCl 2 and heparin, the colloid resistance of blood serum proteins is impaired and the fraction of pre-β- and β-lipoproteins precipitates.
Normal values
Clinical and diagnostic value
An increase in the fractions of β- and pre-β-lipoproteins in the blood serum is closely associated with hypercholesterolemia, which accompanies atherosclerosis, diabetes, hypothyroidism, mononucleosis, some acute hepatitis, severe hypoproteinemia, xanthomatosis, glycogen disease, and is also observed in fatty degeneration of the liver, obstructive jaundice. Burstein's dysproteinemic test is important not only in hyperlipemic conditions, but also as a functional liver test. When compared with the thymol test, this indicator is especially valuable. The thymol test is more sensitive in the initial phase, while the Burshtein test is more sensitive in the final phase of acute hepatitis and post-hepatitis assessment. In combination with a thymol test, it is of great importance for differentiating obstructive jaundice from parenchymal jaundice. In parenchymal jaundice, both tests are positive or thymol is positive, and the test for β-lipoproteins is negative. With mechanical jaundice, the thymol test is negative (if there is no secondary hepatitis), the Burshtein test is sharply positive.
A decrease in the content of β‑lipoproteins is noted in cirrhosis, toxic liver dystrophy, hypofunction of the sympathoadrenal system.
- < Назад
Laboratory diagnostic tests have been used by physicians around the world for many decades. They will never lose their relevance due to their informativeness and high diagnostic value. Rather, on the contrary, every year there are more and more new methods and indicators that replenish the complex diagnostic biochemistry of blood. This analysis allows you to study in detail the constituent components of plasma, evaluate the functional abilities of internal organs and determine specific markers for a number of diseases. The interpretation and interpretation of the results of the main indicators of biochemical analysis are described in this article.
It must be taken into account…
When evaluating any analysis, certain factors must be taken into account that have a natural effect on the magnitude of the indicators obtained. It is always necessary to proceed from an understanding of the main principle of a biochemical blood test. The object of its study is blood plasma - its liquid part, obtained after the separation of formed elements. The composition of plasma and the concentration of certain substances in it is affected by the amount of fluid in the body as a whole and in the vascular bed, in particular. This is especially true in young children.
The pattern is such that against the background of dehydration (insufficient fluid intake or increased losses due to exposure to high temperatures, vomiting, diarrhea, etc.), an artificial increase in blood biochemistry indicators occurs. Conversely, excessive flooding of the body (massive intravenous infusion) causes a false decrease in the true value of the obtained indicators.
Assessment of total protein
Total protein is the totality of all plasma protein molecules, regardless of their molecular weight and structural complexity. Includes albumins, globulins, fibrinogen, highly active plasma immune proteins, fibrinogen and other clotting factors. Determining their concentration makes it possible to assess the intensity and direction of protein metabolism in the body: the predominance of synthesis or decay. Most of all, the amount of total protein is influenced by albumins. The rate of the indicator and the interpretation of the deviations are given in the table.
| The norm of total blood protein is 65-85 g / l | |
| What does the increase mean? | What does the downgrade say? |
The danger of such a condition is an increase in the density and viscosity of the blood, which disrupts the microcirculatory processes in the body and can cause blood clots. |
The danger of such a condition is a violation of the oncotic pressure of the plasma, which causes edema. There is a gradual violation of the structure and functions of all organs and systems. |
Assessment of the bilirubin index
Bilirubin is one of the main pigment compounds in the body. Erythrocytes, spleen, liver and biliary system participate in its formation and circulation. It is extremely toxic to tissues, so its plasma concentration reflects the degree of threat to life and health, as well as the functional ability of the liver to neutralize it. Bilirubin is formed during the breakdown of erythrocytes and hemoglobin in the spleen, from where it is sent to the liver cells for binding with glucuronic acid and neutralization. Through the bile ducts, it is excreted along with the feces.
Of practical interest is the interpretation of the excess of the norm of the bilirubin indicator, which ranges from 8 to 20.5 μmol / l. This is possible with:
- Enhanced destruction of red blood cells under the influence of toxic substances, enlarged spleen, autoimmune and infectious diseases;
- Liver diseases, which are manifested by inflammation or destruction of liver cells, which causes a decrease or loss of their ability to bind bilirubin;
- Violation of the outflow of bile through the biliary tract in the presence of stones in them, an inflammatory process or compression of the pancreatic tumor with localization in the head.
Assessment of ALT and AST indicators
All tissues in which active metabolic processes occur contain many enzymes that speed up metabolism. In this regard, the leader in their number is the liver. Less enzymes in the heart muscle. The most significant enzymes that determine the biochemical analysis are ALT or ALT (alanine aminotransferase) and AST or AsAT (aspartate aminotransferase). These blood enzymes have a high enzymatic activity, therefore, they perform their functions exclusively inside the cells. Normally, a small part of them enters the bloodstream in the process of blood supply and metabolic reactions. This formed the basis for the normal values of ALT and AST, which are 0.1-0.8 µmol/(h*ml) and 0.1-0.45 µmol/(h*ml), respectively.
Of practical interest can only be a decoding of the excess of these standards. This is possible with:
- Toxic effects on the body;
- Inflammation and destruction of liver cells with active hepatitis and the initial stages of cirrhosis (more due to ALT);
- Inflammation and destruction of heart tissue as a result of myocardial infarction (more due to AST).
ALT and AST are not toxic to the body. These indicators are diagnostic markers of diseases of the liver and heart, which are accompanied by massive destruction of cells. Diagnostic significance is acquired by exceeding their norm by two or more times.
Evaluation of indicators of urea and creatinine
To evaluate the results of the direction of protein metabolism in the body, along with the indicator of total protein, allows the determination of the level of creatinine and urea in the blood. Their rate is:
- 50-115 µmol/l for creatinine;
- 4.2-8.3 µmol/l for urea.
Both of these compounds are metabolites formed during protein breakdown. Therefore, almost always decoding is required only when indicators are found that exceed the norm. If so, you can think of:
- Renal pathology, accompanied by renal failure;
- Massive destruction of muscle tissue as a result of trauma, dystrophy, inflammation or circulatory disorders;
- Intoxication and liver diseases;
- Excess consumption of protein and chemical supplements containing protein metabolites.
Evaluation of cholesterol and its fractions
Cholesterol is a metabolite of lipid metabolism. Its physiological role for the body is very large, since it is involved in the synthesis of steroid hormones and cell membranes. It exists in the body in three main forms, which correspond to the name of the biochemistry indicator:
- Free cholesterol - the norm is up to 5.2 mmol / l;
- Low density lipoproteins (LDL) - the norm is up to 2.2 mmol / l;
- High density lipoproteins (HDL) - the norm is 0.9-1.9 mmol / l.
From a practical point of view, it may be interesting to decipher both the increase and decrease in the concentration of these substances in the blood plasma. Registration of indicators of free cholesterol or LDL, exceeding the norm, indicates a high risk of developing atherosclerosis of the vessels. As a rule, this is possible with metabolic disorders as a result of obesity, diabetes mellitus or excessive intake of cholesterol from food. With this increase, there is a decrease in HDL. An increase in the latter is not dangerous, but rather, on the contrary, it is useful, since this type of cholesterol-protein compound is responsible for cleaning the vessels from free cholesterol.
If the indicators of free blood cholesterol obtained in the analyzes are below the standard values, this indicates the depletion of lipid reserves in the body, which threatens to disrupt the synthesis of steroid hormones, primarily sex hormones. The danger of such a condition is that with its long-term preservation, a violation of the structure of the cells of vital organs can occur, which will not be able to restore it.
A biochemical blood test is a powerful tool in the hands of a knowledgeable specialist. Its correct decoding will help to timely diagnose a number of diseases, determine their threats and the effectiveness of the treatment.
Lipoproteins and their role
Blood lipoproteins, due to their biochemical properties, are the main form of transportation of triglycerides and cholesterol esters in our body. Fats, due to their hydrophobicity, cannot move around the body without special carriers.
- Varieties of lipid transporters
- The composition of the lipoprotein molecule
- Ways of transformations of various transport forms of lipids in the body
- Causes of lipoprotein imbalance
- If a lipid imbalance is detected
Fat balance is determined by the ratio between atherogenic and anti-atherogenic fat transporters. In the event of its violation, lipids are deposited in the walls of the arteries, with the subsequent formation of cholesterol deposits, gradually reducing the lumen of the vessels.
Varieties of lipid transporters
The classification of lipoproteins includes five main fractions:
- Very low density lipoproteins (VLDL).
- Intermediate density lipoproteins (ILPP).
- Low density lipoproteins (LDL).
- High density lipoproteins (HDL, also called alpha anti-atherogenic lipoproteins).
- Chylomicrons.
Using special laboratory techniques, it is possible to isolate even up to 15-17 fractions of blood fat carriers.
All of these transport forms are closely interconnected with each other, they interact with each other and can be transformed into each other.
The composition of the lipoprotein molecule
Blood plasma lipoproteins are represented by spherical protein molecules, whose direct function in the body is transport ─ they carry out the transport of cholesterol molecules, triglycerides and other lipids through the bloodstream.
Lipoproteins differ in size, density, properties and functions. Their structure is represented by spherical structures, in the center of which are triglycerides and esterified cholesterol, constituting the so-called hydrophobic core. Around the nucleus is a soluble layer of phospholipids and apoproteins. The latter are agents of interaction with many receptors and ensure that lipoproteins perform their functions.
There are several types of apoproteins:
- Apoprotein A1 ─ ensures the return of cholesterol from tissues to the liver, with the help of this apoprotein, excess cholesterol is utilized. It is the main component of HDL.
- Apoprotein B is the main component of XM, VLDL, LDL and LDL. Provides the ability of these carriers to transfer fats to tissues.
- Apoprotein C is a structural component of HDL.
Ways of transformations of various transport forms of lipids in the body
Chylomicrons are large complexes formed in the intestines from digested fatty acids and cholesterol. Before entering the general circulation, they pass through the lymphatic vessels, where the necessary apoproteins are attached to them. In the blood, chylomicrons are rapidly cleaved under the influence of a specific enzyme (lipoprotein lipase) located in the endothelium of the walls of blood vessels, while a large amount of fatty acids are released, which are absorbed by tissues. In this case, degradation products remain from chylomicrons, which are processed by the liver.
The lifespan of these transport forms of fats ranges from a few minutes to half an hour.
Very low density lipoproteins are synthesized by the liver, their main function is the transport of most endogenously formed triglycerides. After leaving the liver, they take on their surface apoproteins (apoA, apoC, apoE, and others) from HDL. In hyperlipidemia, the liver usually produces more VLDL than required. In addition, elevated VLDL levels are a sign of insulin resistance. The lifetime of VLDL is on average 6-8 hours. Also, like chylomicrons, lipoproteins of this class have an affinity for the endothelium of the vessels of muscle and adipose tissue, which is necessary in order to transfer the fats transported by them. When VLDL lose the main part, which consisted mainly of the triglycerides of its core, during lipolysis, they decrease in size and become intermediate density lipoproteins.
Intermediate density transporters are not always the result of degradation of very low density lipoproteins, some of them come from the liver. They can be of different composition depending on the level of esterified cholesterol and triglycerides present.
Low density lipoproteins exist in the blood for up to 10 hours. May be formed in the liver, may be a product of lipolysis of LPPP. Cholesterol in low-density lipoproteins is transferred to fat-requiring peripheral tissues. Also, together with VLDL, they play a significant role in the development of atherosclerosis.
High density lipoproteins can exist for up to 5 days.
They are engaged in the fact that they capture excess cholesterol from tissues and lipoproteins of other fractions and transfer it to the liver for processing and excretion from the body. There are also several sub-fractions within HDL. The liver is the site of their formation, they are synthesized there independently of other lipoproteins and have a unique set of apoproteins on their surface. This group of lipid transporters is regarded as anti-atherogenic. They exhibit antioxidant and anti-inflammatory properties.
The entire biochemistry of the transformations of fat carriers in the blood would be impossible without capillaries, the endothelium of which contains lipoprotein lipase, which hydrolyzes triglycerides that are part of HM, VLDL, LDL.
Causes of lipoprotein imbalance
Among the main reasons why the balance in fat metabolism is disturbed are the following:
- Muscles are the main consumer of free fatty acids supplied by atherogenic VLDL and LDL. This means that a decrease in physical activity is one of the powerful risk factors for impaired fat metabolism and the appearance of atherosclerotic vascular lesions.
- Chronic stress is also an important factor. It has been studied that during stress, an increased concentration of cortisol in the blood is maintained, while the anabolic hormone insulin is reduced. Against this background, an increase in all components of lipid metabolism is usually recorded, which means a higher risk of diseases of the cardiovascular system.
- Improper nutrition (an abundance of fat in the diet).
- Bad habits (especially smoking).
- Excess weight.
- genetic predisposition.
- Arterial hypertension.
- Diabetes mellitus and other endocrinopathies.
- Diseases of the liver and kidneys.
- Taking certain medications.
If a lipid imbalance is detected
Doctors, determining the ratio of atherogenic lipoproteins and anti-atherogenic fat carriers, determine the so-called atherogenic coefficient. It can be used to assess the risk of progression of atherosclerotic lesions in each individual patient.
The main goal for a doctor in the treatment of a patient is to control blood cholesterol, as well as the correct ratio of individual fractions of transport forms of fats.
To do this, methods of drug correction are used, but the direct participation of the patient himself in improving his well-being and further prognosis is extremely important ─ changing lifestyle and nutrition, combating chronic stress. The patient must understand that victory over the disease is possible only if he does not take a neutral position, but takes the side of the treating doctor.
Lipoproteins or lipoproteins(English) lipoprotein) - complex proteins, consisting of apolipoproteins and lipids. From lipids, lipoproteins may include: free fatty acids, phospholipids, cholesterol, neutral fats, and others. Apolipoproteins (synonyms: apoproteins and apo) are proteins, components of lipoproteins that specifically bind to the corresponding lipids during the formation of a lipoprotein.
In the illustration: the structure of a lipoprotein. Original drawing by AntiSense, licensed under the GNU Free Documentation License. Adapted.
Types of lipoproteins
There are different classifications of lipoproteins, focused on their various characteristics. Lipoproteins are divided into water-soluble (blood plasma, milk, etc.) and structural, which are part of cell membranes, the myelin sheath of nerve fibers, and structural plant tissues.The most famous and widespread is the classification of plasma lipoproteins by density. Allocate:
- Chylomicrons
- Very low density lipoproteins (VLDL or VLDL)
- Low density lipoproteins (LDL or LDL)
- Intermediate (medium) density lipoproteins (LDL, LPP, LSP or LPSP)
- High density lipoproteins (HDL or HDL)
The average values of the characteristics of different classes of lipoproteins (in a population of young healthy people weighing about 70 kg):
| Type | Density, g/ml |
Diameter, nm | % protein | % cholesterol | % phospholipids | % triglycerides and cholesterol esters |
| HDL | >1,063 | 5–15 | 33 | 30 | 29 | 4 |
| LDL | 1,019–1,063 | 18–28 | 25 | 50 | 21 | 8 |
| LPPP | 1,006–1,019 | 25–50 | 18 | 29 | 22 | 31 |
| VLDL | 0,95–1,006 | 30–80 | 10 | 22 | 18 | 50 |
| Chylomicrons | <0,95 | 100-1000 | <2 | 8 | 7 | 84 |
Separately allocate lipoproteins (a)(pictured left) - a subclass of human plasma lipoproteins. Lipoprotein (a) is a separate risk factor for the development of cardiovascular disease. The concentration of lipoprotein (a) in the blood plasma is determined mainly by genetics and exercise, drug therapy or diet has little effect on it.
"Good" and "bad" lipoproteins
High-density lipoproteins are considered to be "good", while low, intermediate and very low density are "bad". In general, the higher the concentration of HDL in plasma, the lower the risk of atherosclerosis and other cardiovascular diseases. With its excess of “bad” lipopoproteins (LDL, LSP and VLDL), plaques appear in the walls of blood vessels, which can limit the movement of blood through the vessel, which threatens atherosclerosis and significantly increases the risk of heart disease (ischemic disease, heart attack) and stroke.HDL easily penetrate the wall of the arteries and easily leave it, thus not affecting the development of atherosclerosis. LDL, LSP and part of VLDL after oxidation are retained in the walls of the arteries. The largest - chylomicrons and large VLDL are not able to penetrate into the arterial wall due to their size and also do not affect the development of atherosclerosis.
To reduce "bad" lipoproteins, a diet (see below) and therapy with drugs from the statin group (atorvastatin, cerivastatin, rosuvastatin, pitavastatin, etc.) can be recommended.
Basic diet for lowering lipids (cholesterol)
| Principles | Sources |
| Decreased total fat and saturated fat intake |
Butter, hard margarine, whole milk, hard and soft cheeses, visible meat fat, duck, goose, regular sausage, cakes, cream, coconut and palm oil |
| Increasing consumption of high-protein, low-saturated fat foods |
Fish, chicken, turkey, game, veal |
| Increased complex carbohydrates and fruit, vegetable and cereal fibers, especially fiber | All fresh frozen vegetables, fresh fruits, all unpolished grains, lentils, dried beans, rice |
| Increasing consumption of polyunsaturated and monounsaturated fats | Sunflower, corn, olive oil, soybean oil and other products from them, if they are not in solid form (not hydrogenated) |
| Dietary cholesterol reduction | Brains, kidneys, tongue, eggs (no more than 1-2 yolks per week), liver (no more than 2 times a month) |
| Reducing sodium intake | Salt, monosodium glutamate, canned vegetables and meat, salty foods (ham, bacon, smoked fish), mineral water with a lot of salt |
Disorders of lipoprotein metabolism in ICD-10
Various disorders of lipoprotein metabolism in ICD-10 are classified as “Class IV. Diseases of the endocrine system, eating disorders and metabolic disorders (E00-E90) ", block" E70-E90 Metabolic disorders ", codes:- "E78.0 Pure hypercholesterolemia" (familial hypercholesterolemia; Fredrickson's hyperlipoporteinemia, type IIa; hyper-beta-lipoproteinemia; hyperlipidemia, group A; hyperlipoproteinemia with low-density lipoprotein)
- E78.1 Pure hyperglyceridemia (endogenous hyperglyceridemia; Fredrickson's hyperlipoporteinemia, type IV; hyperlipidemia, group B; hyperpre-beta lipoproteinemia; hyperlipoproteinemia with very low density lipoproteins)
- E78.2 Mixed hyperlipidemia (extensive or floating beta-lipoproteinemia; Fredrickson's hyperlipoporteinemia, types IIb or III; hyper-beta-lipoproteinemia with pre-beta lipoproteinemia; hypercholesterolemia with endogenous hyperglyceridemia; hyperlipidemia, group C; tuboeruptive xanthoma; tuberous xanthoma )
- E78.3 Hyperchylomicronemia (Fredrickson hyperlipoporteinemia, types I or V; hyperlipidemia, group D; mixed hyperglyceridemia)
- E78.4 Other hyperlipidemias (familial combined hyperlipidemia)
- E78.5 Hyperlipidemia, unspecified
- E78.6 Lipoprotein deficiency (A-beta-lipoproteinemia; high-density lipoprotein deficiency; hypo-alpha-lipoproteinemia; hypo-beta-lipoproteinemia (familial); lecithincholesterol acyltransferase deficiency; Tangier disease)
- "E78.8 Other disorders of lipoprotein metabolism"
- "E78.9 Disorders of lipoprotein metabolism, unspecified"
Medical services related to the determination of the level of lipoproteins in human blood
The Order of the Ministry of Health and Social Development of Russia No. 1664n dated December 27, 2011 approved the Nomenclature of Medical Services. Section 9 of the Nomenclature provides for a number of medical services related to the determination of the level of lipoproteins in human blood:On the site in the "Literature" section there are subsections " Eating disorders and metabolic disorders, obesity, metabolic syndrome" and " Cardiovascular diseases associated with diseases of the gastrointestinal tract", containing articles for healthcare professionals that address these issues.
The results of studies of the level of lipoproteins in the blood provide important information for the attending physician, but they are by no means a diagnosis!
Synthesis, transformation, transport and utilization of fats in the body occurs through the formation of complex compounds. They carry fatty substances through the aqueous medium (cytoplasm of cells, intercellular spaces, plasma), i.e., make them water-soluble. These compounds are lipoproteins, which, depending on the density, are divided into several types. Density is provided by the chemical structure, molecular structure, which all together affects the specifics of the functions they perform.
Therefore, blood lipoproteins are the main indicators of fat metabolism. Based on their ratio in plasma, the risk of developing cardiovascular diseases is calculated. In this regard, lipoproteins are also classified into atherogenic and anti-atherogenic. And to determine their concentration, an analysis of venous blood for a lipid profile is carried out.
There is no difference between lipoprotein and lipoprotein. This is the same
Based on their name, lipoproteins are complexes of fats and proteins.
- Fats are represented by cholesterol and its esters, triglycerides, fat-soluble vitamins and phospholipids. They are used in the construction of cell membranes to ensure their selective permeability, the production of steroid hormones (adrenal cortex, male and female gonads), vitamin D. The fatty components of lipoproteins serve as catalysts for some chemical reactions and the main source of energy. Fats are mostly synthesized by tissues, and only a fifth of them comes from food.
- Protein component represented by apolipoproteins - special proteins specific to each fraction of lipoproteins. They are formed in the human body near the places of synthesis or intake of fats (in the liver, nerve and intestinal epithelial cells). The structure of the carrier protein is designed for the transport of lipids in the aquatic environment: one of its ends, fat-soluble, faces the inside of the compound and is associated with a drop of fat, the other, water-soluble, is brought out, it interacts with the surrounding biological fluid.
It is logical that lipoprotein molecules have a shape close to a ball, where the role of the core performs the fat component, and the role shells- proteinaceous. The transport forms of lipids differ not in their qualitative structure, but in the percentage of substances included in them: the less fats and more proteins in their composition, the denser they are. They also differ in size, and with increasing density, their diameter decreases.
Normally, the biochemistry of lipoproteins is dynamic, and their level is constantly changing. It depends on:
- gender;
- age;
- motor activity;
- prescription of food intake;
- time of day and year;
- hormonal state (puberty, pregnancy, lactation).
The analysis of blood plasma for lipoproteins of each patient is checked against specially developed tables of norms that take into account the main physical parameters. But the main value for assessing lipid metabolism is not so much compliance with normal indicators as the ratio of lipoproteins to each other.
Lipoprotein classification
The “assembly” of lipoproteins is carried out according to the scheme: disparate synthesis of endogenous (own) fats and proteins → combination of fat with a small amount of protein with the formation of very low density lipoproteins → addition of a little more protein with the formation of intermediate density lipoproteins → the next increase in protein with the formation of low density lipoproteins.
Low-density lipoproteins are delivered by the blood to the body tissues in need, are fixed on cell receptors specific to them, release fatty components and attach protein components. Consequently, they condense, resulting in high-density lipoproteins. HDL is disconnected from the receptors, sent to the liver, where it is converted into bile acids, which remove the remnants of unused fat into the intestines for disposal.
If we are talking about exogenous lipids that come with food, then they also bind to protein. But the process stops at the first, and only, stage. The formed lipoproteins are called "chylomicrons", they enter the lymph, and then into the blood.
And now - about each faction separately.
XM (chylomicrons)
These are the largest fat-protein particles, 90% consisting of triglycerides. They are carried by chylomicrons. XM does not play a big role in the metabolism of cholesterol and other lipids.
- Formed in the intestine, chylomicrons enter the lymphatic vessels and are brought into the thoracic lymphatic duct. And from it they are transported into the bloodstream through apoproteins A and B-48.
- In the lumen of blood vessels, primary chylomicrons also borrow apoproteins C II and E from high-density lipoproteins, as a result of which they mature and become full-fledged triglyceride donors.
- Under the influence of the lipase enzyme secreted by the cells of the vascular lining, the compound with three fatty acids breaks down into single 3 fragments. They are used directly in situ or combined with albumin and transported to distant target tissues (muscle, fat, kidney, spleen, bone marrow and lactating mammary gland).
- As a result, very few useful substances remain in the composition of XM. These are residual chylomicrons captured by the liver and used by it for the synthesis of endogenous fats.
Since chylomicrons carry exogenous fats, they can normally be found in the blood only after eating. Then their concentration drops to microdoses, which are not detected during the analysis. Complete elimination ends after 12 hours.
VLDL (very low density)
These compounds are formed in the liver cells as a result of the binding of apoprotein B-100 to lipids synthesized from residual chylomicrons and from glucose. Among them, as in the case of HM, triglycerides predominate, which already account for 65%. The amount of cholesterol and phospholipids, although 3 times more, nevertheless, VLDL are also not their main carriers.
Once in the plasma, VLDL go through the same stages of metabolism as chylomicrons, being similarly enriched in apoproteins C II and E, replenishing the body's fat and energy reserves and turning into residual forms. Mature VLDL is somewhat denser than CM and 2.5–25 times smaller in diameter. They have a weak atherogenicity, but in combination with other risk factors lead to the development of vascular atherosclerosis.
LPPP (intermediate density)
So called residual VLDL. They are the immediate precursors of low-density lipoproteins. LPPP is almost 2 times less than VLDL, all the fatty components in them are approximately equal, apoproteins (E and B-100) already make up ⅕ of the molecule. They don’t tolerate anything: the main function of LDLP is to be a matrix for the synthesis of LDL.
LDL (low density)
Intermediate density lipoproteins are scavenged by the liver and either in the liver cells or in the spaces between them, enriched in cholesterol, phospholipids and apoprotein B-100. The percentage of triglycerides in them is negligible, but cholesterol is already 50%. Therefore, LDL plays a major role in its transfer from the place of production to peripheral tissues.
Low-density lipoproteins penetrate into the cells of the body and break down into components that are used in different directions. "Impoverished" LDL are rich in protein, so their density automatically becomes high.
HDL (high density)
Half of high-density lipoprotein consists of a protein component, ⅕ part is cholesterol, another ⅕ are phospholipids, and quite a bit are triglycerides. Therefore, the transfer of the last HDL is not involved. They provide transport of the cholesterol remaining after participation in the metabolism to the liver cells for utilization, and also supply phospholipids to all cell structures to build their membranes.
In addition, HDL on the way to the liver exchange protein, cholesterol and its esters with other lipoproteins. Being the main transporter of cholesterol to the place of its destruction, high-density lipoproteins were called "good".
The unit of measure for lipoproteins is mmol/l or mg/dl. The lipid profile analysis includes the determination of both the lipoprotein fractions themselves and the total cholesterol for all of them, as well as triglycerides and the atherogenic coefficient (the risk of developing atherosclerotic plaques). The study is carried out on an empty stomach after a 2–3-day sparing diet, limitation of physical and psycho-emotional stress and smoking cessation half an hour before blood sampling.
Violation of the composition of blood lipoproteins
The leading role in the violation of fat metabolism is assigned to "bad" lipoproteins. These include LDL, the main function of which is the incorporation of cholesterol into damaged cytoplasmic membranes. It, like the inner layer of a sandwich panel, strengthens the cell membranes and optimizes their throughput. But with an excess of LDL and damaged vascular lining, cholesterol is deposited in the thickness of the arteries, leading to the formation of atherosclerotic plaques.
Blood lipoproteins, due to their biochemical properties, are the main form of transportation of triglycerides and cholesterol esters in our body. Fats, due to their hydrophobicity, cannot move around the body without special carriers.
Lipoprotein
Fat balance is determined by the ratio between atherogenic and anti-atherogenic fat transporters. In the event of its violation, lipids are deposited in the walls of the arteries, with the subsequent formation of cholesterol deposits, gradually reducing the lumen of the vessels.
Varieties of lipid transporters
The classification of lipoproteins includes five main fractions:
- Very low density lipoproteins (VLDL).
- Intermediate density lipoproteins (ILPP).
- Low density lipoproteins (LDL).
- High density lipoproteins (HDL, also called alpha anti-atherogenic lipoproteins).
- Chylomicrons.
Using special laboratory techniques, it is possible to isolate even up to 15-17 fractions of blood fat carriers.
All of these transport forms are closely interconnected with each other, they interact with each other and can be transformed into each other.
The composition of the lipoprotein molecule
Structure of a lipoprotein
Blood plasma lipoproteins are represented by spherical protein molecules, whose direct function in the body is transport ─ they carry out the transport of cholesterol molecules, triglycerides and other lipids through the bloodstream.
Lipoproteins differ in size, density, properties and functions. Their structure is represented by spherical structures, in the center of which are triglycerides and esterified cholesterol, constituting the so-called hydrophobic core. Around the nucleus is a soluble layer of phospholipids and apoproteins. The latter are agents of interaction with many receptors and ensure that lipoproteins perform their functions.
There are several types of apoproteins:
- Apoprotein A1 ─ ensures the return of cholesterol from tissues to the liver, with the help of this apoprotein, excess cholesterol is utilized. It is the main component of HDL.
- Apoprotein B is the main component of XM, VLDL, LDL and LDL. Provides the ability of these carriers to transfer fats to tissues.
- Apoprotein C is a structural component of HDL.
Ways of transformations of various transport forms of lipids in the body
Chylomicrons are large complexes formed in the intestines from digested fatty acids and cholesterol. Before entering the general circulation, they pass through the lymphatic vessels, where the necessary apoproteins are attached to them. In the blood, chylomicrons are rapidly cleaved under the influence of a specific enzyme (lipoprotein lipase) located in the endothelium of the walls of blood vessels, while a large amount of fatty acids are released, which are absorbed by tissues. In this case, degradation products remain from chylomicrons, which are processed by the liver.
The lifespan of these transport forms of fats ranges from a few minutes to half an hour.
The proteins in lipoproteins are called apoproteins.
Very low density lipoproteins are synthesized by the liver, their main function is the transport of most endogenously formed triglycerides. After leaving the liver, they take on their surface apoproteins (apoA, apoC, apoE, and others) from HDL. In hyperlipidemia, the liver usually produces more VLDL than required. In addition, elevated VLDL levels are a sign of insulin resistance. The lifetime of VLDL is on average 6-8 hours. Also, like chylomicrons, lipoproteins of this class have an affinity for the endothelium of the vessels of muscle and adipose tissue, which is necessary in order to transfer the fats transported by them. When VLDL lose the main part, which consisted mainly of the triglycerides of its core, during lipolysis, they decrease in size and become intermediate density lipoproteins.
Intermediate density transporters are not always the result of degradation of very low density lipoproteins, some of them come from the liver. They can be of different composition depending on the level of esterified cholesterol and triglycerides present.
Low density lipoproteins exist in the blood for up to 10 hours. May be formed in the liver, may be a product of lipolysis of LPPP. Cholesterol in low-density lipoproteins is transferred to fat-requiring peripheral tissues. Also, together with VLDL, they play a significant role in the development of atherosclerosis.
High density lipoproteins can exist for up to 5 days.
They are engaged in the fact that they capture excess cholesterol from tissues and lipoproteins of other fractions and transfer it to the liver for processing and excretion from the body. There are also several sub-fractions within HDL. The liver is the site of their formation, they are synthesized there independently of other lipoproteins and have a unique set of apoproteins on their surface. This group of lipid transporters is regarded as anti-atherogenic. They exhibit antioxidant and anti-inflammatory properties.
The entire biochemistry of the transformations of fat carriers in the blood would be impossible without capillaries, the endothelium of which contains lipoprotein lipase, which hydrolyzes triglycerides that are part of HM, VLDL, LDL.
Causes of lipoprotein imbalance
Risk factors for hypercholestremia
Among the main reasons why the balance in fat metabolism is disturbed are the following:
- Muscles are the main consumer of free fatty acids supplied by atherogenic VLDL and LDL. This means that a decrease in physical activity is one of the powerful risk factors for impaired fat metabolism and the appearance of atherosclerotic vascular lesions.
- Chronic stress is also an important factor. It has been studied that during stress, an increased concentration of cortisol in the blood is maintained, while the anabolic hormone insulin is reduced. Against this background, an increase in all components of lipid metabolism is usually recorded, which means a higher risk of diseases of the cardiovascular system.
- Improper nutrition (an abundance of fat in the diet).
- Bad habits (especially smoking).
- Excess weight.
- genetic predisposition.
- Arterial hypertension.
- Diabetes mellitus and other endocrinopathies.
- Diseases of the liver and kidneys.
- Taking certain medications.
If a lipid imbalance is detected
Doctors, determining the ratio of atherogenic lipoproteins and anti-atherogenic fat carriers, determine the so-called atherogenic coefficient. It can be used to assess the risk of progression of atherosclerotic lesions in each individual patient.
The main goal for a doctor in the treatment of a patient is to control blood cholesterol, as well as the correct ratio of individual fractions of transport forms of fats.
To do this, methods of drug correction are used, but the direct participation of the patient himself in improving his well-being and further prognosis is extremely important ─ changing lifestyle and nutrition, combating chronic stress. The patient must understand that victory over the disease is possible only if he does not take a neutral position, but takes the side of the treating doctor.
