LIPIDS are water-insoluble compounds, therefore, for their transport by the blood, special carriers are needed that are soluble in water. Such transport forms are LIPOPROTEINS. They are classified as free lipids. Synthesized fat in the intestinal wall, or fat synthesized in other tissues of the organs can be transported by the blood only after being included in the composition of LIPOPROTEINS, where proteins play the role of a stabilizer.

According to their structure, LIPOPROTEINS micelles have an outer layer and a core. The outer layer is formed from PROTEINS, PHOSPHOLIPIDS and CHOLESTEROL, which have hydrophilic polar groups and show an affinity for water. The core consists of triglycerides, cholesterol esters, fatty acids, vitamins A, D, E, K. So. insoluble fats are easily transported throughout the body after being synthesized in the intestinal wall and also synthesized in other tissues between the cells that synthesize and use them.

There are 4 classes of blood LIPOPROTEINS, which differ from each other in their chemical state, micelle size and transported fats. Since they have different settling rates in sodium chloride solution, they are divided into:

1. CHylomicrons. Formed in the intestinal wall and have the largest particle size.

2. VLDL. Synthesized in the intestinal wall and liver.

3. LDL. Formed in the endothelium of capillaries from VLDL.

4. HDL. Formed in the intestinal wall and liver.

That. transport blood lipids are synthesized by two types of cells - enterocytes and hepatocytes. It was found that blood lipoproteins during protein electrophoresis move in the zone of alpha and beta - GLOBULINs, so their electrophoretic mobility is still

denoted as:

Pre-beta-LP = VLDL,

Beta-LP=LDL,

Alpha-LP=HDL.

rice. The chemical composition of blood lipoproteins

CHYLOMICRONS (XM) as the largest particles during electrophoresis remain at the start.

Their maximum concentration is reached by 4 - 6 hours after eating. They split

under the action of the enzyme - LIPOPROTEID LIPASE, which is formed in the liver, lungs, adipose tissue

after a meal, XM predominantly transports TRIACYLGLYCERIDES (up to 83%).

VLDL and LDL mainly transport cholesterol and its esters to the cells of organs and tissues. These fractions are classified as ATHEROGENIC. HDL- is commonly referred to as ANTIATHEROGENIC LP, which carry out the transport of CHOLESTEROL (excess cholesterol released as a result of the breakdown of cell membranes) to the liver for subsequent oxidation with the participation of cytochrome P450 with the formation of bile acids, which are excreted from the body in the form of COPROSTEROLS. Blood LIPOPROTEINS disintegrate after endocytosis in LYSOSOMS and MICROSOMES: under the action of LIPOPROTEID LIPASE in the cells of the liver, kidneys, adrenal glands, intestines of adipose tissue, capillary endothelium. Products of LP hydrolysis are involved in cellular metabolism.

Bilirubin total (Bilirubin total)

Blood pigment, a breakdown product of hemoglobin, myoglobin and cytochromes.

Yellow hemochromic pigment, formed as a result of the breakdown of hemoglobin, myoglobin and cytochromes in the reticuloendothelial system of the spleen and liver. One of the main components of bile, is also contained in the serum in the form of two fractions: direct (bound, or conjugated) and indirect (free, or unbound) bilirubin, together making up the total blood bilirubin.

In laboratory diagnostics, the determination of total and direct bilirubin is used. The difference between these indicators is the amount of free (non-conjugated, indirect) bilirubin. During the breakdown of hemoglobin, free bilirubin is initially formed. It is practically insoluble in water, lipophilic, and therefore easily soluble in membrane lipids, penetrating into mitochondrial membranes, disrupting metabolic processes in cells, and is highly toxic. Bilirubin is transported from the spleen to the liver in combination with albumin. In the liver, free bilirubin binds to glucuronic acid. As a result, conjugated (direct), water-soluble, less toxic bilirubin is formed, which is actively excreted into the bile ducts against the concentration gradient.

With an increase in the concentration of bilirubin in the serum over 27 - 34 µmol / l, jaundice appears (mild form - up to 85 µmol / l, moderate - 86 - 169 µmol / l, severe form - over 170 µmol / l). In newborns, physiological jaundice is observed in the first week of life (with an increase in total blood bilirubin due to the fraction of indirect bilirubin), since there is an increased destruction of erythrocytes, and the bilirubin-conjugating system is imperfect. Hyperbilirubinemia may be the result of increased production of bilirubin due to increased hemolysis of erythrocytes (hemolytic jaundice), a reduced ability to metabolize and transport bilirubin against the gradient into bile by hepatocytes (parenchymal jaundice), as well as a consequence of mechanical difficulties in biliary excretion (obstructive - congestive, mechanical, cholestatic jaundice.) .

For the differential diagnosis of jaundice, a complex of pigment tests is used - determining the concentration in the blood of total, direct bilirubin (and assessing the level of indirect bilirubin by their difference), as well as determining the concentration of urobilinogen and bilirubin in the urine.

Bilirubin direct (bilirubin conjugated, bound; Bilirubin direct)

The fraction of total bilirubin in the blood, resulting from the processes of conjugation of free bilirubin in the liver.

This compound of free bilirubin with glucuronic acid is bilirubin glucuronide. Highly soluble in water; penetrates into tissues, low toxicity; gives a direct reaction with a diazo reagent, hence the name "direct" bilirubin (as opposed to unconjugated free "indirect" bilirubin, which requires the addition of a reaction accelerator).

Direct bilirubin is synthesized in the liver and then most of it enters the small intestine with bile. Here, glucuronic acid is split off from it, and bilirubin is restored to urobilin through the formation of mesobilirubin and mesobilinogen (partially this process occurs in the extrahepatic biliary tract and gallbladder). Bacteria in the intestine convert mesobilirubin to stercobilinogen, which is partially absorbed into the blood and excreted by the kidneys, most of it is oxidized to stercobilin and excreted in the feces. A small amount of conjugated bilirubin passes from the liver cells into the blood. In hyperbilirubinemia, direct bilirubin accumulates in elastic tissue, the eyeball, mucosal membranes, and skin.

The growth of direct bilirubin is observed in parenchymal jaundice due to impaired ability of hepatocytes to transport conjugated bilirubin against the gradient into bile. And also with obstructive jaundice due to a violation of the outflow of bile. Patients with elevated serum levels of direct (bound) bilirubin have bilirubinuria.

Cholesterol total (cholesterol, Cholesterol total)

Diagnosis of atherosclerosis, cholesterol, cholesterol level

The most important indicator of lipid metabolism.

Cholesterol (cholesterol) is a secondary monohydric cyclic alcohol. It is found in the blood and tissues of the body in free and esterified forms.

Free cholesterol is a component of cell plasma membranes, as well as mitochondrial and endoplasmic reticulum membranes (in a smaller amount). Its esters predominate in blood serum. Cholesterol is a precursor of sex hormones, corticosteroids, bile acids, and vitamin D.

Up to 80% of cholesterol is synthesized in the liver, and the rest enters the body with animal products (fatty meat, butter, eggs). Cholesterol is insoluble in water, its transport between tissues and organs occurs due to the formation of lipoprotein complexes.

Fractions of low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol are isolated, differing in composition and functions.

The cholesterol level at birth is below 3.0 mmol/L. With age, its level in the blood increases, there are sex differences in concentration. In men, cholesterol levels rise in early and middle age and fall in old age. In women, the concentration of cholesterol increases more slowly with age, up to menopause, in the future it can exceed the level of men. This is due to the action of sex hormones. Estrogens decrease and androgens increase total cholesterol levels.

The accumulation of cholesterol is a risk factor for the development of atherosclerosis and coronary heart disease (CHD). A high risk of developing coronary artery disease in adults - the concentration of cholesterol in the blood is above 6.22 mmol / l. When the concentration of total cholesterol is in the range of borderline values ​​and above, it is advisable to study cholesterol in combination with the determination of triglycerides, HDL and LDL cholesterol.

HDL Cholesterol (High Density Lipoprotein Cholesterol, HDL Cholesterol)

Fraction of lipoproteins responsible for the transport of cholesterol from peripheral cells to the liver.

Lipoproteins in the blood carry out the transport of lipids, including cholesterol, from one cell population to another. Unlike other lipoproteins, HDL transports cholesterol from the cells of peripheral organs (including heart vessels, brain arteries, etc.) to the liver, where cholesterol is converted into bile acids and excreted from the body.

In women, on average, HDL values ​​are higher than in men. A decrease in HDL-cholesterol concentration below 0.90 mmol / l for men and below 1.15 mmol / l for women, as well as a ratio of low-density lipoprotein cholesterol to high-density lipoprotein greater than 3:1 is associated with an increased risk of atherosclerosis.

An elevated level of HDL-cholesterol is considered as an anti-atherogenic factor.

LDL Cholesterol (Low Density Lipoprotein Cholesterol, LDL, Cholesterol LDL)

The fraction of lipoproteins responsible for the transfer of cholesterol to the cells of tissues and organs.

Attention! This study is not performed separately, only in combination with tests: No. 30 (Triglycerides), No. 31 (Total Cholesterol), No. 32 (Cholesterol - HDL).

Low density lipoproteins (LDL) are the main transport form of cholesterol, transporting it mainly in the form of cholesterol esters. They belong to beta lipoproteins.

Lipoproteins in the blood transport lipids, including cholesterol, from one cell population to another. It is believed that the LDL-cholesterol index correlates more with the risk of atherosclerosis than the level of total cholesterol, since it is this fraction that ensures the flow of cholesterol to the vessels and organs. Under conditions of pathology, LDL is captured by cells in the walls of blood vessels with the formation of atherosclerotic plaques, which narrow the lumen of blood vessels and contribute to thrombosis.

An elevated level of LDL-cholesterol (more than 3.37 mmol/l) is considered as a risk factor for the development of atherosclerosis, and a level > 4.14 mmol/l can be regarded as a high risk of atherosclerosis and coronary heart disease.

Triglycerides (Triglycerides)

The main blood lipids, which are the main source of energy for cells.

They enter the body with food, and are also synthesized by cells of adipose tissue, liver, and intestines. They do not circulate in a free form, but are associated with proteins and are transported in the form of macromolecular complexes - lipoproteins. They are the main lipids of body fat and foods. The triglyceride molecule contains triatomic glycerol and 3 residues of higher fatty acids, mainly palmitic, stearic, linoleic and oleic.

The main source of energy for cells. Triglycerides accumulate in fat cells, from where, after hydrolysis, they are broken down to glycerol and fatty acids and released into the circulation system.

Low density lipoproteins (LDL) are cholesterol fractions with high levels of atherogenicity. An elevated level of LDL and VLDL cholesterol indicates the presence or high risk of developing atherosclerotic lesions of the vascular walls, coronary artery disease, acute myocardial infarction and cerebral stroke.

It should be noted that recently there has been a pronounced trend towards rejuvenation of cardiovascular pathologies. If earlier severe vascular atherosclerosis and its complications developed in patients over 55-60 years old, now this pathology also occurs in 25-30 year olds.

Low-density lipoproteins are called fractions of "bad" cholesterol, which have a high level of atherogenicity and lead to the development of atherosclerotic lesions of the vascular walls. In the early stages of lipid imbalance, when low-density lipoproteins are just beginning to accumulate in the vascular intima, HDL is “captured” and transported to the liver, where it is converted into bile acids.

Thus, the natural balance of lipids is maintained in the body. However, with a long-term increase in the level of LDL and a decrease in the amount of HDL, low-density lipoproteins not only accumulate in the vessel wall, but also provoke the development of an inflammatory reaction, accompanied by the destruction of elastin fibers, followed by their replacement with rigid connective tissue.

Why is high LDL dangerous?

The progression of atherosclerosis is accompanied by a significant decrease in the elasticity of the vascular wall, a violation of the ability of the vessel to stretch the blood flow, as well as narrowing of the lumen of the vessel due to an increase in the size of the atherosclerotic plaque (accumulation of LDL, VLDL, etc.). All this leads to impaired blood flow, increased formation of microthrombi and impaired microcirculation.

Depending on the location of the focus of atherosclerotic vascular lesions, symptoms develop:

• IHD (atherosclerosis of the coronary vessels);
• INC (ischemia of the lower extremities due to atherosclerotic lesions of the vessels of the legs and abdominal aorta);
• cerebral ischemia (narrowing of the lumen of the vessels of the neck and brain), etc.

In what cases is the diagnosis of LDL prescribed?

The level of LDL and the risk of developing diseases of the heart and blood vessels has a direct relationship. The higher the level of low-density lipoproteins in the blood, the higher the likelihood of the patient developing severe pathologies of the cardiovascular system.

Carrying out a regular blood test for LDL allows you to detect lipid imbalances in time and choose a lipid-lowering diet for the patient and, if necessary, a scheme for drug correction of cholesterol levels.

This analysis is recommended once a year for all people over 35 years of age. In the presence of risk factors for the development of cardiovascular diseases, preventive examinations can be carried out more often. Also, the analysis is indicated if the patient has:

• obesity;
• diabetes;
• liver diseases;
• thyroid pathologies;
• chronic pancreatitis and cholecystitis;
• complaints of shortness of breath, constant muscle weakness, fatigue, dizziness, memory loss;
• complaints of pain in the legs, aggravated by walking, shifting lameness, constant chilliness of the feet and hands, pallor or redness of the legs, etc.

Low-density lipoproteins in a blood test are also evaluated during pregnancy. It should be noted that a moderate increase in cholesterol levels during childbearing is normal and does not require treatment. However, with a significant increase in the level of low density lipoproteins, the risk of spontaneous abortion, impaired feto-placental blood flow, pregnancy fading, intrauterine growth retardation, premature birth, etc. increases.

Reduced levels of LDL and HDL cholesterol during pregnancy may also indicate a high risk of developing late toxicosis, as well as bleeding during childbirth.

Risk factors for the development of atherosclerosis and pathologies of the cardiovascular system

As a rule, LDL cholesterol is elevated in:

• smokers;
• patients who abuse alcohol, fatty, fried and smoked foods, sweets, flour, etc.;
• patients with obesity, diabetes;
• persons leading a sedentary lifestyle;
• patients suffering from insomnia and frequent stress;
• patients with a burdened family history (relatives with early cardiovascular pathologies).

Also, LDL in the blood increases in the presence of chronic pathologies of the liver, pancreas, beriberi, hereditary lipid disorders, etc.

Indications for LDL testing

The lipid profile is assessed:

• to confirm or refute the presence of atherosclerotic vascular lesions;
• in a comprehensive examination of patients with diseases of the liver, pancreas, jaundice, as well as pathologies of the endocrine system;
• when examining patients with suspected hereditary lipid disorders;
• to assess the risks of coronary artery disease and determine the coefficient of atherogenicity.

Calculation of the coefficient of atherogenicity is used to assess the ratio of the amount of total cholesterol (TC) and high density lipoproteins, as well as the risk of developing severe atherosclerotic vascular lesions. The higher the ratio, the higher the risk.

Atherogenic coefficient = (OH-HDL) / HDL.

Normally, the ratio of HDL and total cholesterol (LDL + VLDL and HDL) ranges from 2 to 2.5 (the maximum allowable values ​​for women are -3.2, and for men - 3.5).

The norm of low density lipoproteins

The norms of LDL content depend on the gender of the patient and his age. The rate of LDL in the blood of women during pregnancy increases depending on the period of bearing the child. There may also be a slight difference in indicators when taking tests in different laboratories (this is due to the difference in equipment and reagents used). In this regard, the assessment of the level of LDL in the blood should be carried out exclusively by a specialist.

How to get tested for LDL cholesterol?

Blood sampling should be done in the morning, on an empty stomach. Smoking is prohibited half an hour before the analysis. It also excludes physical and emotional stress.

A week before the study, it is necessary to exclude the intake of alcohol and food rich in cholesterol.

LDL norm in men and women

Gender differences in the analyzes are due to the difference in the hormonal background. In women before menopause, high levels of estrogen lower blood LDL cholesterol. This contributes to the formation of natural hormonal protection against atherosclerosis and cardiovascular pathologies. In men, due to the prevalence of androgens, the level of LDL in the blood is slightly higher than in women. Therefore, they are much more likely to have severe atherosclerosis at an early age.

LDL cholesterol levels in the table by age for men and women:

Patient's age	Floor	LDL mmol/l
From 5 to 10	M	1,63 — 3,34
	AND	1,76 — 3,63
From 10 to 15 tons	M	1,66 — 3,44
	AND	1,76 — 3,52
From 15 to 20	M	1,61 — 3,37
	AND	1,53 — 3,55
From 20 to 25	M	1,71 — 3,81
	AND	1,48 — 4,12
From 25 to 30	M	1,81 — 4,27
	AND	1,84 — 4,25
From 30 to 35	M	2,02 — 4,79
	AND	1,81 — 4,04
From 35 to 40	M	2,10 — 4,90
	AND	1,94 — 4,45
From 40 to 45	M	2,25 — 4,82
	AND	1,92 — 4,51
From 45 to 50	M	2,51 — 5,23
	AND	2,05 — 4,82
From 50 to 55	M	2,31 — 5,10
	AND	2,28 — 5,21
From 55 to 60	M	2,28 — 5,26
	AND	2,31 — 5,44
From 60 to 65	M	2,15 — 5,44
	AND	2,59 — 5,80
From 65 to 70	M	2,54 — 5,44
	AND	2,38 — 5,72
More than 70	M	2,28 — 4,82
	AND	2,49 — 5,34

What does it mean if low density lipoproteins are elevated

LDL cholesterol is elevated in patients with:

• various hereditary lipid disorders (hypercholesterolemia and hypertriglyceridemia);
• overweight;
• severe renal pathologies (the presence of nephrotic syndrome, renal failure);
• jaundice, obstructive nature;
• endocrine pathologies (diabetes mellitus, hypothyroidism, adrenal disease, polycystic ovary syndrome, etc.);
• nervous exhaustion.

The cause of falsely elevated low-density cholesterol in the analyzes may be the use of various drugs (beta-blockers, diuretics, glucocorticosteroid hormones, etc.).

LDL cholesterol is lowered

Reduced LDL levels can be observed in patients with hereditary hypolipidemia and hypotriglyceridemia, chronic anemia, malabsorption in the intestine (malabsorption), myeloma, severe stress, chronic pathologies of the respiratory tract, etc.

Also, the intake of drugs cholestyramine ® , lovastatin ® , thyroxine ® , estrogens, etc. leads to a decrease in lipid levels.

How to lower LDL cholesterol levels in the blood

All lipid-lowering therapy should be prescribed by the attending physician based on the results of the tests. As a rule, statins (lovastatin®, simvastatin®), bile acid sequestrants (cholestyramine®), fibrates (clofibrate®), etc. are prescribed.

How to lower LDL cholesterol without drugs?

Diet and lifestyle changes are carried out as a mandatory addition to drug therapy. As independent methods of treatment, they can be used only in the early stages of atherosclerosis.

Cholesterol is a lipoprotein, and in the human body is present in the blood and in cell membranes. Blood cholesterol is represented by cholesterol esters, and in membranes - free cholesterol. Cholesterol is a vital substance, as it is involved in the formation of bile, sex hormones, and gives firmness to the cell membrane. The notion that cholesterol = harm is wrong. More dangerous for the body is the lack of cholesterol than its excess. However, an excess amount of cholesterol in the blood is a prerequisite for the development of such a disease as atherosclerosis. Therefore, the determination of cholesterol is a marker for the development of atherosclerosis.

How to take a blood test for cholesterol?

To determine the lipid profile, blood from a vein taken in the morning on an empty stomach is used. Preparation for the test is usual - refraining from food for 6-8 hours, avoiding physical exertion and rich fatty foods. The determination of total cholesterol is carried out by the unified international method of Abel or Ilk. The determination of fractions is carried out by precipitation and photometry methods, which are rather laborious, but accurate, specific and quite sensitive.

The author warns that the norm indicators are averaged, and may differ in each laboratory. The material of the article should be used as a reference and no attempt should be made to make a diagnosis and start treatment on your own.

Lipidogram - what is it?
Today, the concentration of the following blood lipoproteins is determined:

1. total cholesterol
2. High density lipoproteins (HDL or α-cholesterol),
3. Low density lipoproteins (LDL beta cholesterol).
4. Triglycerides (TG)

The combination of these indicators (cholesterol, LDL, HDL, TG) is called lipidogram. A more important diagnostic criterion for the risk of developing atherosclerosis is an increase in the LDL fraction, which is called atherogenic, that is, contributing to the development of atherosclerosis.

HDL, on the contrary, are antiatherogenic fraction, as they reduce the risk of atherosclerosis.

Triglycerides are a transport form of fats, so their high content in the blood also leads to the risk of atherosclerosis. All these indicators together or separately are used to diagnose atherosclerosis, coronary artery disease, as well as to determine the risk group for the development of these diseases. Also used as a treatment control.

Read more about coronary heart disease in the article: angina pectoris

"Bad" and "good" cholesterol - what is it?

Let us examine in more detail the mechanism of action of cholesterol fractions. LDL is called "bad" cholesterol, since it is he who leads to the formation of atherosclerotic plaques on the walls of blood vessels, which interfere with blood flow. As a result, due to these plaques, vessel deformation occurs, its lumen narrows, and blood cannot pass freely to all organs, as a result, cardiovascular insufficiency develops.

HDL, on the contrary, is “good” cholesterol, which removes atherosclerotic plaques from the walls of blood vessels. Therefore, it is more informative and correct to determine cholesterol fractions, and not just total cholesterol. After all, total cholesterol is made up of all fractions. For example, the concentration of cholesterol in two people is 6 mmol / l, but one of them has 4 mmol / l for HDL, while the other has the same 4 mmol / l for LDL. Of course, a person who has a higher HDL concentration can be calm, and a person who has a higher LDL should take care of his health. Here is such a possible difference, with seemingly the same level of total cholesterol.

Lipidogram norms - cholesterol, LDL, HDL, triglycerides, atherogenic coefficient

Consider lipid profile indicators - total cholesterol, LDL, HDL, TG.
An increase in blood cholesterol levels is called hypercholesterolemia.

Hypercholesterolemia occurs as a result of an unbalanced diet in healthy people (heavy consumption of fatty foods - fatty meat, coconut, palm oil) or as a hereditary pathology.

The norm of blood lipids

The atherogenic coefficient (KA) is also calculated, which is normally less than 3.

Atherogenic coefficient (KA)

KA shows the ratio of atherogenic and anti-atherogenic fractions in the blood.

How to calculate KA?

This is easy to do just by having lipid profile results. It is necessary to divide the difference between total cholesterol and HDL cholesterol by the HDL value.

Deciphering the values ​​​​of the coefficient of atherogenicity

• If KA of atherosclerosis is minimal.
• If KA is 3-4, then the content of atherogenic fractions is higher, then there is a high degree of probability of developing atherosclerosis and coronary heart disease (CHD),
• If KA> 5 - indicates that a person has a high probability of atherosclerosis, which significantly increases the likelihood of vascular diseases of the heart, brain, limbs, kidneys

Read more about atherosclerosis in the article: Atherosclerosis

In order to normalize fat metabolism, it is necessary to strive for the following blood indicators:

What do lipid profile abnormalities indicate?

Triglycerides

TG is also referred to as risk factors for the development of atherosclerosis and coronary artery disease (ischemic heart disease). When the concentration of TG in the blood is more than 2.29 mmol / l, we are talking about the fact that the person is already sick with atherosclerosis or coronary artery disease. With a blood TH concentration in the range of 1.9-2.2 mmol / l (border values), it is said that atherosclerosis and coronary artery disease are developing, but these diseases themselves have not yet fully developed. An increase in the concentration of TG is also observed in diabetes mellitus.

LDL

An LDL concentration above 4.9 mmol / l indicates that a person is sick with atherosclerosis and coronary artery disease. If the concentration of LDL lies in the range of borderline values ​​of 4.0-4.9 mmol / l, then atherosclerosis and coronary artery disease are developing.

HDL

HDL in men is less than 1.16 mmol / l, and in women less than 0.9 mmol / l is a sign of the presence of atherosclerosis or coronary artery disease. With a decrease in HDL to the area of ​​\u200b\u200bboundary values ​​(in women 0.9-1.40 mmol / l, in men 1.16-1.68 mmol / l), we can talk about the development of atherosclerosis and coronary artery disease. An increase in HDL suggests that the risk of developing coronary artery disease is minimal.

Read about the complication of atherosclerosis - stroke in the article:

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 the 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.

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.