Lipoproteins are a complex of lipids with proteins that are part of any living organism. Lipoproteins take part in the functions of transport and storage of lipids and are considered an integral component of the morphological structure of the cell.
During diagnostic testing to identify various diseases, specialists often pay attention to the percentage of lipid-protein complexes in the body.
In addition, beta lipoproteins and alpha lipoproteins can be used in establishing paternity or in forensic practice to identify physical evidence. Lipoproteins can be free, soluble in an aqueous environment, or structural.
Lipoproteins play an important role in the human body. Thanks to transport proteins, cholesterol dissolves in the blood plasma and begins to move throughout the body. Cholesterol enters the body not only from food. Almost 80% of the component fat metabolism produced in the liver.
Cholesterol takes an active part in the synthesis of sex hormones and has a strengthening and protective effect on cell membranes. In addition, the fat metabolism component contributes to the restoration of cell membranes and the production of vitamin D.
Molecules loaded with cholesterol are much larger than those that lack it. The mass of cholesterol affects the density of the molecule. The higher the mass, the greater the density. According to the level of density, lipoproteins are divided into the following categories:
High blood cholesterol may be a consequence of taking sex hormones or contraceptives
A disturbance in the exchange of HDL and LDL should be a reason to visit a doctor.
The main purpose of lipoproteins is considered to be the transportation of cholesterol in the body. However, in addition to this, they take an active part in the transport of carotenoids and triglycerides. Due to the dissolution of beta lipoproteins in the blood plasma, a precipitate is formed, which begins to settle on the walls of blood vessels.
At normal quantity cholesterol in the body, the sediment can be independently processed and removed from the circulatory system. With elevated cholesterol levels, atherosclerotic plaques begin to appear and grow, leading to stroke and heart attack.
In order to find out the level of b lipoproteins in the body, you should donate blood for a biochemical analysis, which displays the amount of cholesterol in the blood. In addition to biochemistry, the patient mandatory receives a referral for a lipid profile that recognizes cholesterol fractions that are in the human circulatory system.
A lipid profile is prescribed when as a last resort when there is a suspicion of elevated cholesterol levels, which can be bad or good. If there is a sharp decrease in the concentration of high-density lipoproteins, it is worth undergoing additional examinations in order to exclude the development of atherosclerosis.
To assess the risk of developing coronary disease heart and determine treatment tactics, lipoprotein analysis should be performed high degree together with the total cholesterol indicator.
Risk level for developing cardiovascular diseases
The level of beta lipoproteins in the blood should be kept under control. If the readings are elevated, you should consult a doctor who will prescribe treatment. To determine the risk of developing coronary heart disease, it is important to correctly calculate the atherogenic coefficient using the formula K = total cholesterol - HDL / HDL. It is worth considering that HDL has antiatherogenic properties.
Norm of atherogenic coefficient in units:
The atherogenicity index in individuals who suffer from coronary heart disease will reach 4-6.
The results of the studies should be studied by the attending physician. It is worth remembering that in people who have had heart attacks or strokes, the norm of low-density lipoproteins will be slightly lower. In addition, the presence of:
The blood collection process is quick and painless
High cholesterol or hypercholesterolemia leads to the formation of atherosclerotic plaques.
The main indication for taking a cholesterol test is age category patient. In older people, cholesterol tends to accumulate in excessive amounts. It is better to start controlling your own health from the age of 20-30. Blood sampling for biochemistry to detect elevated levels of lipoproteins should be carried out every 12 months.
In addition, additional indications for conducting a biochemical blood test include the presence of a hereditary factor (in the case where close relatives of the patient suffer from high cholesterol, we can talk about hereditary susceptibility to these ailments), excess body weight, heart disease, diabetes mellitus, high blood pressure.
Blood sampling from a vein must be done in a special laboratory. It is very important to take the test on an empty stomach (it is advisable not to eat 12-14 hours before the planned hour of the test). During this period of time, you should drink clean water, thanks to which you can get the most accurate cholesterol readings.
Experts have developed a number of rules that must be followed if there is a need to donate blood for biochemistry. 48 hours before blood sampling, you should refuse physical activity and eliminate all kinds of stressful situations. If the patient’s profession involves heavy physical labor, it is recommended to take a week’s break from work and only then go to the medical laboratory.
A recent history of acute respiratory viral infection or influenza should be a reason to postpone testing for 40-50 days. It is worth remembering that while carrying a child, cholesterol levels drop sharply, and after the birth of the baby, real readings can be achieved only 60-90 days after birth.
When using medications, it is important to inform your doctor about this so that he can understand whether any drug has an effect on the biochemistry result. To achieve the most accurate result, it is important to eat right the entire week before blood collection. You will have to completely give up fatty foods during this period of time.
Cholesterol does not dissolve in water, so low-density lipoproteins and special protein compounds are used to transport it
When prescribing therapy, the doctor must take into account the individual characteristics of the body. It is not advisable to use medications when the level of lipoproteins is at the permissible limit or slightly exceeds it.
In this case, the following will help restore health:
By following all the doctor’s recommendations, you can quickly restore your health. If there is an increase in lipoproteins, medications that contain a statin and help block the production of compounds by the liver may be prescribed. Treatment will also be required in cases where the levels are low.
Diet therapy plays a huge role in the treatment of dyslipoproteinemia. Patients are advised to limit their intake of animal fats or replace them with synthetic fats by eating up to 5 small meals a day. The diet should be enriched with vitamins and fiber. You should give up fatty and fried foods, replace meat with sea fish, and have a lot of vegetables and fruits. Regenerative therapy and sufficient physical activity improve the general condition of patients.
The main lipids in human blood plasma are triglycerides (denoted as TG), phospholipids and cholesteryl esters (denoted as cholesterol). These compounds are esters of long-chain fatty acids and, as a lipid component, are collectively included in the composition of lipoproteins (lipoproteins).
All lipids enter the plasma in the form of macromolecular complexes - lipoproteins (or lipoproteins). They contain certain apoproteins (protein part) that interact with phospholipids and free cholesterol, which form outer shell, protecting the triglycerides and cholesterol esters located inside. Normally, in fasting plasma, the majority (60%) of cholesterol is found in low-density lipoprotein (LDL), and less in very low-density lipoprotein (VLDL) and high-density lipoprotein (HDL). Triglycerides are transported primarily by VLDL.
Apoproteins perform several functions: they help the formation of cholesterol esters by interacting with phospholipids; activate lipolysis enzymes such as LCAT (lecithin cholesterol acyltransferase), lipoprotein lipase and hepatic lipase, bind to cell receptors to capture and break down cholesterol.
There are several types of apoproteins:
Apoproteins of the A family (apo A-I and apo A-II) are the main protein components of HDL, and when both apoproteins A are nearby, apo A-P enhances the lipid-binding properties of apo A-I, the latter has another function - activation of LCAT. Apoprotein B (apo B) is heterogeneous: apo B-100 is found in chylomicrons, VLDL and LDL, and apo B-48 is found only in chylomicrons.
Apoprotein C has three types: apo C-1, apo C-II, apo C-III, which are contained mainly in VLDL, apo C-II activates lipoprotein lipase.
Apoprotein E (apo E) is a component of VLDL, LDLP and HDL, and performs several functions, including a receptor - indirect transfer of cholesterol between tissues and plasma.
Chylomicrons are the largest but lightest particles, containing mainly triglycerides, as well as small amounts of cholesterol and its esters, phospholipids and protein. After settling on the surface of the plasma for 12 hours, they form a “creamy layer”. Chylomicrons are synthesized in epithelial cells small intestine from lipids food origin, through the system of lymphatic vessels, CM enter the thoracic lymphatic duct, and then into the blood, where they undergo lipolysis under the action of plasma lipoprotein lipase and are converted into remnants (remnants) of chylomicrons. Their concentration in blood plasma after administration fatty foods increases rapidly, reaching a maximum after 4-6 hours, then decreases, and after 12 hours they are not detectable in the plasma of a healthy person.
The main function of chylomicrons is to transport dietary triglycerides from the intestine into the bloodstream.
Chylomicrons (CMs) deliver dietary lipids into the plasma through the lymph. Under the influence of extrahepatic lipoprotein lipase (LPL), activated by apo C-II, chylomicrons in the plasma are converted into remnant chylomicrons. The latter are taken up by the liver, which recognizes the surface apoprotein E. VLDL transport endogenous triglycerides from the liver to the plasma, where they are converted into DILI, which are either taken up by the LDL receptor in the liver that recognizes apo E or apo B100, or are converted into LDL containing apo B-100 (but there is no longer apo E). LDL catabolism also occurs in two main ways: they carry cholesterol to all cells of the body and, in addition, can be taken up by the liver using LDL receptors.
HDL have a complex structure: the lipid component includes free cholesterol and phospholipids, released during lipolysis of chylomicrons and VLDL, or free cholesterol coming from peripheral cells, from where it is taken up by HDL; the protein component (apoprotein A-1) is synthesized in the liver and small intestine. Newly synthesized HDL particles are present in plasma as HDL-3, but are then converted to HDL-2 by LCAT activated by apo A-1.
VLDL (pre-beta lipoproteins) are similar in structure to chylomicrons, smaller in size, contain less triglycerides, but more cholesterol, phospholipids and protein. VLDL is synthesized mainly in the liver and serves to transport endogenous triglycerides. The rate of VLDL formation increases with an increase in the flow of free fatty acids into the liver and with an increase in their synthesis in the event of a large amount of carbohydrates entering the body.
The protein part of VLDL is represented by a mixture of apo C-I, C-II, C-III and apo B100. VLDL particles vary in size. VLDL undergo enzymatic lipolysis, which results in the formation of small particles - remnant VLDL or intermediate density lipoproteins (IDL), which are intermediate products of the conversion of VLDL to LDL. Large VLDL particles (they are formed when there is an excess of dietary carbohydrates) turn into such LDLPs, which are removed from the plasma before they have time to become LDL. Therefore, with hypertriglyceridemia, a decrease in cholesterol levels is observed.
Plasma VLDL levels are determined using the formula triglycerides/2.2 (mmol/l) and triglycerides/5 (mg/dl).
The normal level of very low density lipoprotein (VLDL) in blood plasma is 0.2 - 0.9 mmol/l.
DILP are intermediate particles formed during the conversion of VLDL into LDL and in composition are something between them - in healthy people the concentration of DILI is 10 times less than the concentration of LDL, and is neglected in studies. The main functional proteins of DILI are apo B100 and apo E, with the help of which DILI bind to the corresponding liver receptors. They are detected in significant quantities in plasma by electrophoresis at III type hyperlipoproteinemia.
LDL (beta lipoproteins) is the main class of plasma lipoproteins that transport cholesterol. These particles contain fewer triglycerides compared to VLDL and only one apoprotein apo B100. LDL are the main carriers of cholesterol to the cells of all tissues, connecting to certain receptors on the cell surface, and play a leading role in the mechanism of agerogenesis, being modified as a result of peroxidation.
The normal level of low-density lipoproteins (LDL) in blood plasma is 1.8-3.5 mmol/l
The norm is determined using the Friedwald formula when the triglyceride concentration is not higher than 4.5 mmol/l: LDL = cholesterol (total) - VLDL - HDL
HDL (alpha lipoproteins) are divided into two subclasses: HDL-2 and HDL-3. The protein part of HDL is represented mainly by apo A-I and apo A-II and in a smaller amount by apo C. Moreover, it has been proven that apo C is very quickly transferred from VLDL to HDL and back. HDL is synthesized in the liver and small intestine. The main purpose of HDL is to remove excess cholesterol from tissues, including from the vascular wall and macrophages to the liver, from where it is excreted from the body as part of bile acids, therefore HDL performs an antiatherogenic function in the body. HDL-3 is disc-shaped and begins to actively take up cholesterol from peripheral cells and macrophages, turning into HDL-2, which is spherical and rich in cholesteryl esters and phospholipids.
The normal level of high-density lipoprotein (HDL) in blood plasma is 1.0 - 1.8 mmol/l in men and 1.2 - 1.8 mmol/l in women.
Several enzymes are actively involved in the metabolism of lipoproteins.
The main enzymes of lipoprotein metabolism:
Lipoprotein lipase is found in adipose tissue and skeletal muscle, where it is associated with glycosamyoglycans localized on the surface of the capillary endothelium. The enzyme is activated by heparin and apo C-II protein, its activity decreases in the presence of protamine sulfate and sodium chloride. Lipoprotein lipase is involved in the breakdown of chylomicrons (CM) and VLDL. Hydrolysis of these particles occurs predominantly in the capillaries of adipose tissue, skeletal muscles and myocardium, resulting in the formation of remnant and DILI. The content of lipoprotein lipase in women is higher in adipose tissue than in skeletal muscle and is directly proportional to the level of HDL cholesterol, which is also higher in women.
In men, the activity of this enzyme is more pronounced in muscle tissue and increases against the background of regular physical activities, parallel to the increase in HDL content in the blood plasma.
Hepatic lipase is located on the surface of liver endothelial cells facing the lumen of the vessel; it is not activated by heparin. This enzyme is involved in converting HDL-2 back to HDL-3 by breaking down triglycerides and phospholipids into HDL-3.
With the participation of DILI and LP, triglyceride-rich lipoproteins (chylomicrons and VLDL) are converted into cholesterol-rich lipoproteins (LDL and HDL).
LCAT is synthesized in the liver and catalyzes the formation of cholesterol esters in the plasma by transferring a saturated fatty acid (usually linoleic) from the HDL3 molecule to the free cholesterol molecule. This process is activated by the apo A-1 protein. The resulting LPVGT particles contain mainly cholesterol esters, which are transported to the liver, where they undergo breakdown,
HMG-CoA reductase is found in all cells capable of synthesizing cholesterol: cells of the liver, small intestine, gonads, and adrenal glands. With the participation of this enzyme, endogenous cholesterol is synthesized in the body. The activity of HMG-CoA reductase and the rate of endogenous cholesterol synthesis decreases with excess LDL and increases in the presence of HDL.
Blocking HMG-CoA reductase activity with medicines(statins) leads to a decrease in the synthesis of endogenous cholesterol in the liver and stimulation of receptor-associated LDL uptake in plasma, which will result in a decrease in the severity of hyperlipidemia.
The main function of the LDL receptor is to provide all cells in the body with cholesterol, which they need to synthesize cell membranes. In addition, it is a substrate for the formation of bile acids, sex hormones, corticosteroids, and therefore most of all
LDL receptors are found in the cells of the liver, gonads, and adrenal glands.
LDL receptors are located on the surface of cells; they “recognize” apo B and apo E, which are part of lipoproteins, and bind LDL particles to the cell. Bound LDL particles penetrate into the cell and are destroyed in lysosomes to form apo B and free cholesterol.
LDL receptors also bind LDLP and one of the subclasses of HDL, which has apo E. HDL receptors have been identified in fibroblasts, smooth muscle cells, and also in liver cells. Receptors bind HDL to the cell, “recognizing” apoprotein A-1. This connection is reversible and is accompanied by the release of free cholesterol from the cells, which is removed from HDL tissues in the form of cholesterol ester.
Plasma lipoproteins constantly exchange cholesterol esters, triglycerides, and phospholipids. Evidence has been obtained that the transfer of cholesteryl esters from HDL to VLDL and triglycerides in the opposite direction is carried out by a protein present in plasma called cholesteryl ester transfer protein. The same protein removes cholesterol esters from HDL. The absence or deficiency of this transfer protein leads to the accumulation of cholesterol esters in HDL.
Triglycerides are esters of fatty acids and glycerol. Fats supplied with food are completely broken down in the small intestine, and here “food” triglycerides are synthesized, which in the form of chylomicrons (CM) enter through the thoracic lymphatic duct into the general bloodstream. Normally, over 90% of triglycerides are absorbed. Endogenous triglycerides (that is, those synthesized from endogenous fatty acids) are also formed in the small intestine, but their main source is the liver, from where they are secreted in the form of very low-density lipoproteins (VLDL).
The half-life of triglycerides in plasma is relatively short, they are quickly hydrolyzed and taken up by various organs, mainly adipose tissue. After eating a fatty meal, triglyceride levels rise quickly and remain high for several hours. Normally, all chylomicron triglycerides should be cleared from the bloodstream within 12 hours. Thus, measuring fasting triglyceride levels reflects the amount of endogenous triglycerides found in plasma.
The normal level of triglycerides in blood plasma is 0.4-1.77 mmol/l.
The two main phospholipids in blood plasma are:
Phospholipid synthesis occurs in almost all tissues, but the main source of phospholipids is the liver. Lecithin comes from the small intestine as part of CM. Most phospholipids that enter the small intestine (for example, in the form of complexes with bile acids) undergo hydrolysis pancreatic lipase. In the body, phospholipids are part of all cell membranes. There is a constant exchange of lecithin and sphingomyelin between plasma and red blood cells. Both of these phospholipids are present in plasma as components of lipoproteins, in which they maintain triglycerides and cholesteryl esters in a soluble state.
The level of serum phospholipids varies from 2 to 3 mmol/l, and in women it is slightly higher than in men.
Cholesterol is a sterol containing a four-ring steroid core and a hydroxyl group. In the body it exists in free form and in the form of an ester with linoleic or oleic acid. Cholesterol esters are mainly formed in plasma by the enzyme lecithin cholesterol acyltransferase (LCAT).
Free cholesterol is a component of all cell membranes; it is necessary for the synthesis of steroid and sex hormones and the formation of bile. Cholesterol esters are predominantly found in the adrenal cortex, plasma and atheromatous plaques, as well as in the liver. Normally, cholesterol is synthesized in cells, mainly in the liver with the participation of the enzyme beta-hydroxy-methylglutaryl-coenzyme A reductase (HMG-CoA reductase). Its activity and the amount of synthesized endogenous cholesterol in the liver are inversely proportional to the level of cholesterol in the blood plasma, which in turn depends on the absorption of dietary cholesterol (exogenous) and the reabsorption of bile acids, which are the main metabolites of cholesterol.
Normally, the level of total plasma cholesterol varies from 4.0 to 5.2 mmol/l, but, unlike the level of triglycerides, it does not increase sharply after consuming fatty foods.
Beta lipoproteins are low-density lipoproteins (LDL), also called “bad cholesterol.” This is the most atherogenic class of lipoproteins: high levels of LDL are associated with increased risk development of atherosclerosis. Therefore, determining the concentration of beta (b) lipoproteins has important diagnostic value.
Beta lipoproteins are the main transport form of cholesterol. The sterol itself is not water soluble. Therefore, pure cholesterol cannot travel independently through the blood plasma. For transport, the synthesized sterol binds to very low or low density lipoproteins. The latter form contains much more sterol than the former.
The structure of beta (b) lipoproteins in blood plasma has next view. The LDL core is formed by a hydrophobic component, mainly cholesterol. The outer shell consists of apolipoprotein B molecule, phospholipids. The second name for LDL comes from the type of protein - beta lipoproteins. Apolipoprotein B stabilizes the lipoprotein molecule and is also the point of adhesion to LDL receptors.
LDL is synthesized by the liver from very low-density lipoproteins rich in triglycerides. The hydrolysis process is accompanied by a decrease in the concentration of triglycerides and an increase in cholesterol levels.
The dimensions of the LDL molecule are 18-26 nm. The smallest particles (19-20.5 nm), called B particles, are associated with more high risk development of coronary heart disease, cerebral hemorrhage (stroke). A-particles or alpha are larger (20.6-22 nm) and do not tend to settle on the walls of blood vessels. This pattern is explained by the easier penetration of small particles into the endothelium of the arteries.
Beta lipoproteins are normally responsible for delivering synthesized cholesterol from the liver to tissues. If a cell requires a sterol, it forms an LDL receptor on its surface. A lipoprotein floating by begins to stick to it with apolipoprotein. The cell then absorbs LDL and releases cholesterol from it.
Recent studies have shown that beta lipoproteins help the body resist infection by Staphylococcus aureus. The mechanism of the process is not completely clear and requires clarification.
For beta lipoproteins, the norm changes with age and depends on gender. Adult men have higher levels of LDL cholesterol than women. With age, the concentration of beta lipoproteins (LDL) increases.
| Age, years | Floor | LDL, mmol/l |
|---|---|---|
| 5-10 | m | 1.64-3.35 |
| and | 1.77-3.64 | |
| 10-15 | m | 1.67-3.45 |
| and | 1.77-3.53 | |
| 15-20 | m | 1.62-3.38 |
| and | 1.54-3.56 | |
| 20-25 | m | 1.72-3.82 |
| and | 1.49-4.13 | |
| 25-30 | m | 1.82-4.28 |
| and | 1.85-4.26 | |
| 30-35 | m | 2.03-4.78 |
| and | 1.82-4.05 | |
| 35-40 | m | 2.11-4.91 |
| and | 1.95-4.46 | |
| 40-45 | m | 2.26-4.83 |
| and | 1.93-4.52 | |
| 45-50 | m | 2.52-5.24 |
| and | 2.06-4.83 | |
| 50-55 | m | 2.32-5.11 |
| and | 2.29-5.22 | |
| 55-60 | m | 2.29-5.27 |
| and | 2.32-5.45 | |
| 60-65 | m | 2.16-5.45 |
| and | 2.58-5.81 | |
| 65-70 | m | 2.55-5.45 |
| and | 2.39-5.73 |
The level of cholesterol and LDL depends on the physiological state of the body. This applies to women, since they experience cyclical fluctuations in the concentration of hormones that affect lipoprotein levels. Throughout menstrual cycle LDL cholesterol levels rise and fall.
Beta lipoproteins are elevated during pregnancy. The concentration of LDL is especially strong, and cholesterol levels increase by the third trimester. This is an absolutely normal phenomenon, which can be explained hormonal changes body.
An increase in beta lipoproteins is not accompanied by symptoms until the atherosclerotic plaque formed by them blocks a significant part of the vessel. Therefore, all adults are recommended to check their cholesterol, LDL, LDL, and triglyceride levels every 4-6 years.
Patients with diabetes mellitus, patients with high blood pressure, hereditary predisposition To the development of coronary heart disease, smokers are at increased risk. They need to monitor the level of cholesterol fractions much more often.
Beta lipoproteins in the blood are determined using laboratory diagnostics. To do this, it is necessary to draw blood from a vein. LDL analysis is rarely performed separately from other lipid fractions. Usually, cholesterol, LDL, LDL, and triglyceride levels are checked at the same time. This comprehensive study called .
A blood test for beta lipoproteins does not require complex preparation. It is necessary to follow the rules common to all biochemical studies:
Elevated beta lipoproteins may be a symptom of a disease or a result Not healthy image life. The main causes of abnormally high LDL levels are:
Elevated LDL levels develop while taking diuretics, beta blockers, oral contraceptives, androgens, progestins, glucocorticoids.
Beta lipoprotein analysis is used to determine the risk of cardiovascular complications of atherosclerosis: myocardial infarction, stroke, ischemia. High LDL helps detect fat metabolism disorders when it takes years for the first symptoms to appear.
Gradation of risks depending on the concentration of LDL.
| Concentration | Risk level | |
|---|---|---|
| mg/dl | mmol/l | |
| less than 50 | less than 1.3 | Optimal level, low risk of coronary heart disease |
| 51-69 | 1,3-1,79 | The optimal level of LDL, at which the rate of progression of atherosclerosis is minimal. This level is recommended to be achieved by people who have clinical picture development of diseases. |
| 70-99 | 1,8-2,59 | Low LDL levels correspond to a low rate of progression of atherosclerosis. |
| 100-129 | 2,6-3,3 | Moderate levels of LDL, corresponding to a high rate of development of atherosclerosis. |
| 130-159 | 3,3-4,1 | Borderline LDL level corresponding to the average risk of developing cardiovascular pathologies. |
| 160-199 | 4,1-4,9 | High LDL levels are associated with a high risk of complications. |
| more than 200 | more than 4.9 | Very high risk. |
In some conditions and diseases, LDL levels may be lowered. If a corresponding blood test reveals a decrease in beta lipoproteins below normal, this indicates:
Beta lipoproteins are lowered when taking cholestyramine, neomycin, lovastatin, thyroxine, interferon, and estrogens.
You can avoid it if you follow simple rules:
People prone to developing atherosclerosis need to be more attentive to their health. Regular examinations and following the doctor’s recommendations will help you maintain your health for as long as possible, notice a deterioration in your health in time, and take action.
Last updated: August 22, 2019
Lipoproteins (lipoproteins, LP) are complex transport forms of complexes consisting of proteins and lipids (fats and fat-like substances).
These complexes are an important component of any body cells and perform the function of transporting elements throughout the body.
They deliver lipids to all tissues and organs of the human body.
An analysis of lipoprotein levels is an important component if you suspect diseases associated with disorders of cholesterol in the blood. Deviations in blood lipid levels may indicate pathological conditions of the body of varying severity.
This group is a class of complex molecules containing indicators of LDL (low-density lipoprotein), HDL (high-density lipoprotein), VLDL (very low-density lipoprotein), phospholipids, neutral fats and fatty acids.
Every cell in the human body contains lipoprotein cells. Lipids play a significant role in many processes in the human body.
Lipoproteins are the main form of movement of lipids throughout the body. Since lipids do not dissolve, they cannot fulfill their purpose on their own.
In the blood, lipids bind to a protein called apoprotein, which leads to the solubility of the former and the formation of a new substance called lipoprotein.
Lipoprotein plays a major role in the body's transport system and lipid metabolism.
Transportation of substances entering the human body with consumables food products fats is the main function of chylomicrons. VLDL are transporters of triglycerides to the site of disposal, and with the help of LDL, cholesterol is delivered to the cells of the body.
Reduces the risk of disease progression, with normal indicators, HDL level.
Another important function of LP is to increase the permeability of cell membranes. This will allow you to maintain your metabolism within normal limits.
The protein part of lipoproteins is represented by globulins, which activate immune system the body, and also force the blood to clot and transport iron to the tissues.
The classification of this type of cell occurs depending on its density. It is the most common.
There are four types of drugs:
The chemical composition of all lipoproteins is equal, but the proportional content relative to each other is different.
There is also a classification of lipoproteins, according to which they are divided into:
Today in medicine there are four types of lipoprotein, each of which is determined by the indicators of a biochemical blood test. Let's consider each of them separately.
This indicator not registered when healthy condition body and is observed only in cases of lipid metabolism disorders. The synthesis of these lipids occurs in the small intestine, where they are produced by the mucous membrane, or rather its epithelial cells.
They are responsible for transporting exogenous fat from the small intestine to tissues and the liver.
The predominant part of transported fats are triglycerides, the rest are cholesterol and phospholipids.
Under the influence of enzymes in the liver, triglycerides are broken down and fatty acids are formed, one part of which is combined with albumin, and the other moves to adipose and muscle tissue.
Transporting cholesterol from tissues to the liver is the main task of high-density lipoproteins. Their components are phospholipids, which help maintain cholesterol concentrations within normal limits and prevent it from leaving the blood.
HDL synthesis occurs in the liver cavity and their main task is to transport cholesterol from tissues to the liver cavity for disposal.
This type of cholesterol is also called “good”, since it is not capable of accumulating and increasing cholesterol levels above normal.
An increase in the indicators of this type of lipoprotein is recorded with excessive overweight, death of liver tissue and a condition of the liver in which more than 5% of the liver mass is fat, mainly triglycerides.
The HDL complex also increases during alcohol intoxication.
Its indicators are reduced, mainly with atherosclerotic (cholesterol) deposits on the walls of blood vessels, as well as with rare hereditary disease when a low state of “good” cholesterol appears.
This type of lipoprotein is also called “bad” cholesterol. Low-density lipoproteins transport endogenous cholesterol, triglycerides and phospholipids from the liver directly to tissues.
This type of lipoprotein contains up to forty-five percent cholesterol and is responsible for its transport properties. Low density cholesterol is formed in the blood by the action of lipoprotein lipase on VLDL.
This indicator is the most significant for diagnosing cholesterol problems.
When total cholesterol levels are normal, and this indicator is elevated, this indicates a disruption in fat metabolism and the risk of progression of the deposition of atherosclerotic plaques on the walls of blood vessels.
It is these lipids that can be deposited on the walls of blood vessels, provoking the development of atherosclerosis.
LDL levels are elevated in women and men, due to a pathological increase in lipids in the blood, low production of thyroid hormones, as well as nephrotic syndrome, which is characterized by edema, a small amount of proteins and a high concentration of lipids in the blood.
The decline in low-density lipoproteins occurs when inflammatory processes pancreas, during the period of bearing a child, with a pathological condition of the kidneys and/or liver, as well as with acute forms of infectious lesions of the human body.
This type of lipoprotein is synthesized by liver tissues. The main task of these lipids is to move endogenous lipids, which are produced in the liver from carbohydrates, throughout the body to the tissues of the body.
They are the largest lipoproteins, second in size only to chylomicrons. The main part of them is triglycerides and most of cholesterol. If the blood composition contains large number VLDL, the blood becomes more milky and cloudy.
This type of lipid is also a “bad” one, of which internal walls vessels, cholesterol deposits form, narrowing the lumen of the vessel and disrupting blood flow, which leads to the development of serious pathological conditions and even death.
Atherogenic, with the largest number cholesterol, these are VLDL and LDL.
They are able to penetrate the vessel wall and form accumulations. If the metabolic rate is disrupted, then the level of LDL and total cholesterol increases significantly, which is recorded in a blood test.
The remaining varieties of lipoprotein classes transport cholesterol, which plays a very important role in the functioning of the body, into cells. It is responsible for the functions of forming sex hormones, synthesizing vitamin D (extremely important for the normal absorption of calcium), as well as in the process of forming bile.
There are two types of cholesterol, the ratio of which is important 50 to 50:
Cholesterol and LP, role in the body and norms
With deviations in the processes of synthesis of lipoproteins and their removal from the blood, dyslipoproteinemia (DLP) progresses.
A deviation in the lipoprotein ratio is not pathological, but indicates the progression of the disease, in which the walls of blood vessels narrow and the blood supply to the internal organs is disrupted.
An increase in cholesterol in the blood indicates the progression of atherosclerosis, which is a deadly disease.
As dyslipoproteinemia progresses as the underlying disease, it is determined by a genetic predisposition.
The progression of DLP can be a secondary disease, that is, it can progress due to the presence of the following factors:
Lipoprotein reference values
The manifestation of clinical signs when the concentration of lipoproteins is disturbed is due to one of the processes into which dislipoproteinemia is divided. Each of them exhibits different symptoms. Every second inhabitant of planet Earth shows signs of dyslipoproteinemia.
With this form of DLP, there is a high concentration of lipoproteins in the blood, the increase of which was facilitated by both disturbances in the production of cholesterol by the body and when it is consumed with food.
Against the background of the underlying disease, hyperlipoproteinemia progresses as a secondary complication.
In certain pathological conditions of the immune system, lipoproteins are perceived by the body as foreign cells, and the production of antibodies against them begins.
As a result, lipoproteins interact with antibodies, which has a higher cholesterol level than the lipoproteins themselves.
The manifestation of this disorder is characterized by the following symptoms:
Type of hyperlipoproteinemia; Inherent symptoms
| 1st type | · Dense nodules (xanthomas) are formed, which contain cholesterol and are localized over the tendons, |
| Simultaneous increase in the size of the liver and spleen, | |
| · Inflammation of the pancreas, | |
| · Poor general patient's condition, | |
| · Increase body temperature, | |
| Loss of appetite | |
| · Pain in the abdomen, which is characterized by attacks (especially after eating), | |
| 2nd type | Formation of dense nodules in the area of the tendons of the feet, |
| · The appearance of flat enlarged xanthomas in the area around the eyes, | |
| 3rd type | Symptoms of abnormal heart function (pallor, increased sweating, cyanosis, painful sensations in the heart area, cold extremities, etc.), |
| · Formation of pigmentation on the palms, | |
| · The appearance of ulcers in the area above the elbows and knees, | |
| Symptoms of vascular damage lower limbs(cold fingers, blue discoloration, lameness, pain, low walking endurance). | |
| 4th type | · Increased liver size, |
| Progression of cardiac ischemia (insufficient blood supply to the myocardium), | |
| · Obesity. |
This form of DLP is characterized by its hereditary factor with a violation of certain genes.
The manifestation of this form of lipoprotein metabolism disorder is manifested in the following symptoms:
With this form of DLP, the level of LP in the blood is below normal. Most often, this form does not show any clinical signs.
The following factors can serve as provocateurs:
When found the slightest symptoms you should immediately go to the hospital for full examination and possible early diagnosis.
A superficial diagnostic method, when it is possible to determine the deviation of cholesterol from the norm, is a biochemical blood test (BAC).
This blood test provides extensive information about the state of the human body, each organ separately and the metabolic processes and synthesis of blood elements.
Such laboratory blood testing helps to identify hidden pathological conditions and the progression of diseases in the initial stages.
In addition to its other indicators, the LHC also considers lipoproteins of different densities. The level of total cholesterol in the blood is determined by the indicators of lipoproteins of different densities.
But for diagnosing diseases, it will be more important to consider the indicators fractionally, that is, each separately.
When registering elevated levels“bad” cholesterol, additional hardware examinations are prescribed to diagnose the deposition of atherosclerotic plaques.
To obtain the most accurate results, it is necessary to follow measures to prepare for the analysis so that the results do not turn out to be false.
Also, deviations in results also occur in the presence of concomitant diseases of an infectious type (even recently suffered), poisoning, respiratory infections and during the period of childbearing by expectant mothers.
For a more accurate study of lipoproteins, there is a separate blood test called a lipid profile.
A lipidogram is a blood test that determines quantitative indicator lipids in the human body.
In simple words, LPG is a blood test that helps determine the amount of cholesterol and other substances containing fats. This study helps to most accurately assess the degree of risk of progression of atherosclerosis.
Research using lipid profile analysis implies a more detailed and focused study of lipid parameters than in a simple biochemical blood test.
That's why this analysis is much more effective for diseases associated with impaired cholesterol concentration.
Each of the indicators listed below is included in the lipid profile:
The following formula is used for measurement:
The higher the final coefficient, the greater the risk of progression of pathologies of the heart and blood vessels.
Subgroups; Excess body weight; Obesity of the first degree; Obesity of the second degree
| General HS (mmol/l) |
<,0.56 (9.16%) |
<,0.52 (8.61%) |
<,2,0 (25.51%) |
| HDL (mmol/l) |
0 | <,0.02 (1.91%) |
<,0.12 (11.0%) |
| VLDL (mmol/l) |
<,0.14 (14,26%) |
<,0.01 (0.69%) |
<,0.84 (21.27%) |
| LDL (mmol/l) |
<,0.42 (10,67%) |
<,0.54 (13.51%) |
** |
| TG (mmol/l) |
<,0.31 (14,47%) |
<,0.02 (11.05%) |
<,1.9 (22.11%) |
| KA (Units) | <,0.36 (8,66%) |
<,0.45 (10.67%) |
<,1,13 (18.79%) |
An appointment for lipid spectrum analysis can occur both to determine the risk of progression of diseases associated with cholesterol deposits, and to monitor and adjust therapy for already diagnosed diseases.
Among the pathological conditions for which a lipogram is necessary: insufficient blood supply to the heart (caused by atherosclerotic deposits in the coronary arteries), diabetes mellitus, and a constant increase in blood pressure (caused by narrowing of the pulmonary artery).
Also, a lipid profile is indicated for people who are prescribed a diet with reduced amount cholesterol, and taking medications to reduce the quantitative concentration of cholesterol deposits.
The analysis is shown with for preventive purposes from 18 years old - once every five years, and after forty years - once a year.
The use of diet plays a very important role in the treatment of dyslipoproteinemia. It is recommended to adhere to the following diet, which reduces the amount of fat consumed in food.
Consumption of animal fats must be replaced with unsaturated fatty acids, which are concentrated in plant products. It is also recommended to consume more foods rich in vitamin B and iodine.
Your daily diet should contain the following foods:
The use of the above products, in combination with effectively prescribed therapy, will help achieve the desired result.
Before prescribing medications, a diet is usually used for 1-2 months, and after that, if the atherogenic coefficient remains at a high level, medications are used. If the patient suffers from cardiac ischemia, then medications are prescribed immediately.
Treatment should be comprehensive and consist of proper diet and effective therapy.
In many cases, the following drugs are prescribed:
Drugs; Characteristic
| Statins | Most effective drugs medicines of this group are considered. Their effect on cholesterol deposits does not cause side effects and is effective. With the help of statins, the general health of a person is improved, the amount of cholesterol is reduced and an anti-inflammatory effect occurs. |
| (Lovastatin, Fluvastatin, Mevacor, Zocor, Lipitor) | |
| Fibrates | Reduce triglyceride levels and increase HDL levels. |
| (Fenofibrate, Ciprofibrate) | |
| Sequestrants | By removing cholesterol from the body and reducing its synthesis. |
| (Cholestyramine, Colestipol, Cholestipol, Cholestan) | |
| Vitamin complexes | Maintains the general condition of the body. |
| (Aevit, Vitamin C and B, Biovital, Ascorutin) |
If an imbalance of lipoproteins occurs as a result of an initial disease, then the main measures are aimed at eliminating it, after which lipoprotein levels should return to normal.
For prevention normal condition lipoproteins and to restore them, preventive measures must be taken.
These include:
Further prognosis in case of disturbances in lipoprotein levels depends on how quantitatively the plasma LP indicators have increased.
If the level is slightly elevated, this, in most cases, does not indicate pathological condition, and is well corrected through the use of preventive actions and diet.
In the case of an average increase in lipoprotein levels, drug treatment is used in combination with proper nutrition and way of life. It is also necessary additional research vessels, for their narrowing.
If all the doctor’s requirements are met and medications are taken in a timely manner, cholesterol is normalized and returns to normal.
If you do not take prescribed medications, or if they are not effective, as well as if you do not follow a diet and a healthy lifestyle, complications occur. The level of lipid profile indicators becomes the highest, which indicates serious condition body.
Complications with atherosclerotic plaques serious, and if the vessel is completely blocked by a plaque, hypoxia occurs in the organs to which the vessel led.
Gradual tissue death occurs, in the absence of surgical intervention possible severe consequences(heart attack, stroke, gangrene, complete death of organs), which consequently lead to death.
