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 lipid transport 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 assessment of the post-hepatitis state. 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.
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One of the causes of diabetes is high cholesterol levels in the blood. There is also an inverse relationship, when cholesterol levels increase significantly in diabetes, which leads to the occurrence of cardiovascular pathologies.
Cholesterol is part of lipoproteins, which are a kind of vehicle that delivers fats to tissues. To control the health of a diabetic patient, the level of lipoproteins in the blood is necessarily studied, so pathological changes in the body can be noticed and prevented.
Functions and meaning
Lipoproteins (lipoproteins) are complex compounds of lipids and apolipoproteins. Lipids are necessary for the life of the body, but they are insoluble, so they cannot perform their functions on their own.
Apolipoproteins are proteins that bind to insoluble fats (lipids) to form soluble complexes. Lipoproteins transport various particles throughout the body - cholesterol, phospholipids, triglycerides. Lipoproteins play an important role in the body. Lipids are a source of energy, and also increase the permeability of cell membranes, activate a number of enzymes, participate in the formation of sex hormones, the functioning of the nervous system (transmission of nerve impulses, muscle contractions). Apolipoproteins activate blood clotting processes, stimulate the immune system, and are a supplier of iron for body tissues.
Classification
Lipoproteins are classified by density, composition of the protein part, flotation rate, particle size, electrophoretic mobility. Density and particle size are related to each other - the higher the density of the fraction (compounds from protein and fat), the lower its size and lipid content.
Using the ultracentrifugation method, high molecular weight (high density), low molecular weight (low density), low molecular weight lipoproteins (very low density) and chylomicrons are detected.
Classification by electrophoretic mobility includes fractions of alpha lipoproteins (HDL), beta lipoproteins (LDL), per-beta lipoproteins (VLDL), migrating to the globulin zones and chylomicrons (ChM), which remain at the start.
According to the hydrated density, intermediate density lipoproteins (IDL) are added to the above fractions. The physical properties of the particles depend on the composition of the protein and lipids, as well as on their ratio with each other.
Kinds
Lipoproteins are synthesized in the liver. Fats that enter the body from the outside enter the liver as part of chylomicrons.
There are the following types of protein-lipid complexes:
- HDL (high-density compounds) are the smallest particles. This fraction is synthesized in the liver. It contains phospholipids that keep cholesterol from leaving the bloodstream. High density lipoproteins carry out the reverse movement of cholesterol from peripheral tissues to the liver.
- LDL (low-density compounds) larger than the previous faction. In addition to phospholipids and cholesterol, it contains triglycerides. Low density lipoproteins deliver lipids to tissues.
- VLDL (very low compound density) are the largest particles, second in size only to chylomicrons. The fraction contains a lot of triglycerides and "bad" cholesterol. Lipids are delivered to peripheral tissues. If a large amount of per-beta-lipoproteins circulates in the blood, then it becomes cloudy, with a milky tint.
- XM (chylomicrons) produced in the small intestine. These are the largest particles containing lipids. They deliver fats that have entered the body with food to the liver, where triglycerides are further broken down into fatty acids and added to the protein component of the fractions. Chylomicrons can enter the blood only with very significant disorders of fat metabolism.
LDL and VLDL are atherogenic lipoproteins. If these fractions predominate in the blood, then this leads to the formation of cholesterol plaques on the vessels, which cause the development of atherosclerosis and concomitant cardiovascular pathologies.
VLDL elevated: what does it mean in diabetes
In the presence of diabetes mellitus, there is an increased risk of atherosclerosis due to the high content of low molecular weight lipoproteins in the blood. With a developing pathology, the chemical composition of plasma and blood changes, and this leads to a violation of the functions of the kidneys and liver.
Failures in the work of these organs lead to an increase in the level of low and very low density lipoproteins circulating in the blood, while the level of high-molecular complexes decreases. If the levels of LDL and VLDL are elevated, what does this mean and how to prevent a violation of fat metabolism can only be answered after diagnosing and identifying all the factors that provoked an increase in protein-lipid complexes in the bloodstream.
The importance of lipoproteins for diabetics
Scientists have long established the relationship between glucose levels and cholesterol levels in the blood. In diabetics, the balance of fractions with "good" and "bad" cholesterol is significantly disturbed.
Especially clearly this interdependence of metabolism is observed in people with type 2 diabetes. With good control of the level of monosaccharides of type 1 diabetes, the risk of developing cardiovascular diseases decreases, and with the second type of pathology, regardless of such control, HDL still remains at a low level.
When VLDL is elevated in diabetes, what this means for human health can be said by the degree of neglect of the pathology itself.
The fact is that diabetes itself negatively affects the functioning of various organs, including the heart. If, in the presence of concomitant disorders, atherosclerosis of the vessels is added, then this can lead to the development of a heart attack.
Dyslipoproteinemia
In diabetes mellitus, especially if left untreated, dyslipoproteinemia develops - an ailment in which there is a qualitative and quantitative violation of protein-lipid compounds in the bloodstream. This happens for two reasons - the formation in the liver of predominantly low or very low density lipoproteins and the low rate of their excretion from the body.
Violation of the ratio of fractions is a factor in the development of chronic vascular pathology, in which cholesterol deposits form on the walls of the arteries, as a result of which the vessels thicken and narrow in the lumen. In the presence of autoimmune diseases, lipoproteins become foreign agents for immune cells, to which antibodies are produced. In this case, antibodies further increase the risk of developing vascular and heart diseases.
Lipoproteins: the norm for diagnosis and methods of treatment for deviations
In diabetes, it is important to control not only the level of glucose, but also the concentration of lipoproteins in the blood. To determine the coefficient of atherogenicity, to identify the number of lipoproteins and their ratio by fractions, as well as to find out the level of triglycerides, cholesterol, you can use a lipidogram.
Diagnostics
An analysis for lipoproteins is performed by taking blood from a vein. Before the procedure, the patient should not eat for twelve hours. One day before the analysis, you should not drink alcohol, and one hour before the study, it is not recommended to smoke. After taking the material, it is examined by the enzymatic method, in which the samples are stained with special reagents. This technique allows you to accurately determine the quantity and quality of lipoproteins, which allows the doctor to correctly assess the risk of developing atherosclerosis of the vessels.
Cholesterol, triglycerides and lipoproteins: the norm in men and women
In men and women, normal levels of lipoproteins differ. This is due to the fact that the coefficient of atherogenicity in women is reduced due to the increased elasticity of blood vessels, which is provided by estrogen, the female sex hormone. After the age of fifty, lipoproteins, the norm for both men and women, become the same.
HDL (mmol/l):
- 0.78 - 1.81 - for men;
- 0.78 - 2.20 - for women.
LDL(mmol/l):
- 1.9 - 4.5 - for men;
- 2.2 - 4.8 - for women.
Total cholesterol (mmol/l):
- 2.5 - 5.2 - for men;
- 3.6 - 6.0 - for women.
Triglycerides, unlike lipoproteins, have elevated normal rates in men:
- 0.62 - 2.9 - for men;
- 0.4 - 2.7 - for women.
How to interpret test results correctly
The coefficient of atherogenicity (KA) is calculated by the formula: (Cholesterol - HDL) / HDL. For example, (4.8 - 1.5) / 1.5 \u003d 2.2 mmol / l. - this coefficient is low, that is, the likelihood of developing vascular diseases is low. If the value exceeds 3 units, we can talk about the presence of atherosclerosis in the patient, and if the coefficient is equal to or exceeds 5 units, then the person may have pathologies of the heart, brain or kidneys.
Treatment
In case of violation of the metabolism of lipoproteins, the patient should first of all adhere to a strict diet. It is necessary to exclude or significantly limit the consumption of animal fats, enrich the diet with vegetables and fruits. Products should be steamed or boiled. It is necessary to eat in small portions, but often - up to five times a day.
Equally important is constant physical activity. Walking, exercising, playing sports are useful, that is, any active physical activity that will help reduce the level of fat in the body.
For patients with diabetes, it is necessary to control the amount of glucose in the blood by taking sugar-lowering medications, fibrates and satins. In some cases, insulin therapy may be required. In addition to medications, you need to stop drinking alcohol, smoking and avoid stressful situations.
Lipoproteins are complex protein-lipid complexes that are part of all living organisms and are a necessary part of cellular structures. Lipoproteins perform a transport function. Their content in the blood is an important diagnostic test, signaling the degree of development of diseases of the body systems.
This is a class of complex molecules, which can simultaneously include free, fatty acids, neutral fats, phospholipids and in various quantitative ratios.
Lipoproteins deliver lipids to various tissues and organs. They consist of non-polar fats located in the central part of the molecule - the core, which is surrounded by a shell formed from polar lipids and apoproteins. The similar structure of lipoproteins explains their amphiphilic properties: simultaneous hydrophilicity and hydrophobicity of the substance.
Functions and meaning
Lipids play an important role in the human body. They are found in all cells and tissues and are involved in many metabolic processes.
lipoprotein structure
- Lipoproteins are the main transport form of lipids in the body.. Since lipids are insoluble compounds, they cannot fulfill their purpose on their own. Lipids bind in the blood to proteins - apoproteins, become soluble and form a new substance called lipoprotein or lipoprotein. These two names are equivalent, abbreviated - LP.
Lipoproteins occupy a key position in the transport and metabolism of lipids. Chylomicrons transport fats that enter the body with food, VLDL deliver endogenous triglycerides to the site of disposal, cholesterol enters cells with the help of LDL, HDL have antiatherogenic properties.
- Lipoproteins increase the permeability of cell membranes.
- LP, the protein part of which is represented by globulins, stimulate the immune system, activate the blood coagulation system and deliver iron to the tissues.
Classification
LP of blood plasma is classified by density(using the ultracentrifugation method). The more lipids are contained in the LP molecule, the lower their density. Allocate VLDL, LDL, HDL, chylomicrons. This is the most accurate of all existing drug classifications, which was developed and proven using an accurate and rather painstaking method - ultracentrifugation.
The size of the LP is also heterogeneous. The largest molecules are chylomicrons, and then in decreasing size - VLDL, HDL, LDL, HDL.
Electrophoretic classification LP is very popular among clinicians. Using electrophoresis, the following classes of LP were identified: chylomicrons, pre-beta lipoproteins, beta lipoproteins, alpha lipoproteins. This method is based on the introduction of an active substance into a liquid medium using a galvanic current.
Fractionation LP is carried out in order to determine their concentration in blood plasma. VLDL and LDL are precipitated with heparin, while HDL remains in the supernatant.
Kinds
Currently, the following types of lipoproteins are distinguished:
HDL (high density lipoprotein)
HDL transports cholesterol from body tissues to the liver.
- An increase in HDL in the blood is noted with obesity, fatty hepatosis and biliary cirrhosis, alcohol intoxication.
- A decrease in HDL occurs with hereditary Tangier disease, caused by the accumulation of cholesterol in tissues. In most other cases, a decrease in the concentration of HDL in the blood is a sign.
HDL levels are different for men and women. In males, the LP value of this class ranges from 0.78 to 1.81 mmol / l, the norm for women HDL is from 0.78 to 2.20, depending on age.
LDL (low density lipoprotein)
LDL are carriers of endogenous cholesterol, triglycerides and phospholipids from the liver to tissues.
This class of LP contains up to 45% cholesterol and is its transport form in the blood. LDL is formed in the blood as a result of the action of the enzyme lipoprotein lipase on VLDL. With its excess, they appear on the walls of the vessels.
Normally, the amount of LDL is 1.3-3.5 mmol / l.
- The level of LDL in the blood rises with hypothyroidism, nephrotic syndrome.
- A reduced level of LDL is observed with inflammation of the pancreas, hepatic-renal pathology, acute infectious processes, pregnancy.
infographics (click to enlarge) - cholesterol and LP, role in the body and norms
VLDL (very low density lipoproteins)
VLDL are formed in the liver. They carry endogenous lipids synthesized in the liver from carbohydrates into tissues.
These are the largest LPs, second in size only to chylomicrons. They are more than half composed of triglycerides and contain a small amount of cholesterol. With an excess of VLDL, the blood becomes cloudy and acquires a milky hue.
VLDL is a source of "bad" cholesterol, from which plaques form on the vascular endothelium. Gradually plaques increase, joins with the risk of acute ischemia. VLDL is elevated in patients with kidney disease.
Chylomicrons
Chylomicrons are absent in the blood of a healthy person and appear only in violation of lipid metabolism. Chylomicrons are synthesized in the epithelial cells of the small intestine mucosa. They deliver exogenous fat from the intestine to peripheral tissues and the liver. Most of the transported fats are triglycerides, as well as phospholipids and cholesterol. In the liver, under the influence of enzymes, triglycerides break down and fatty acids are formed, some of which are transported to muscles and adipose tissue, and the other part binds to blood albumins.
what do major lipoproteins look like
LDL and VLDL are highly atherogenic- containing a lot of cholesterol. They penetrate the wall of the arteries and accumulate in it. When metabolism is disturbed, the level of LDL and cholesterol rises sharply.
The most safe against atherosclerosis are HDL. Lipoproteins of this class remove cholesterol from cells and contribute to its entry into the liver. From there, it enters the intestines with bile and leaves the body.
Representatives of all other classes of LP deliver cholesterol to cells. Cholesterol is a lipoprotein that is part of the cell wall. It is involved in the formation of sex hormones, the process of bile formation, the synthesis of vitamin D, which is necessary for the absorption of calcium. Endogenous cholesterol is synthesized in the liver tissue, adrenal cells, intestinal walls, and even in the skin. Exogenous cholesterol enters the body along with animal products.
Dyslipoproteinemia - a diagnosis in violation of lipoprotein metabolism
Dyslipoproteinemia develops when two processes are disturbed in the human body: the formation of LP and the rate of their excretion from the blood. H violation of the ratio of LP in the blood is not a pathology, but a factor in the development of a chronic disease, in which the arterial walls are compacted, their lumen narrows and the blood supply to the internal organs is disturbed.
With an increase in the level of cholesterol in the blood and a decrease in the level of HDL, atherosclerosis develops, leading to development of deadly diseases.
Etiology
Primary dyslipoproteinemia is genetically determined.
Causes secondary dyslipoproteinemias are:
- hypodynamia,
- Diabetes,
- Alcoholism,
- kidney dysfunction,
- hypothyroidism,
- hepatic-renal failure,
- Long-term use of certain medications.
The concept of dyslipoproteinemia includes 3 processes - hyperlipoproteinemia, hypolipoproteinemia, alipoproteinemia. Dyslipoproteinemia is quite common: every second inhabitant of the planet has similar changes in the blood.
Hyperlipoproteinemia is an increased content of LP in the blood due to exogenous and endogenous causes. The secondary form of hyperlipoproteinemia develops against the background of the underlying pathology. In autoimmune diseases, LP are perceived by the body as antigens, to which antibodies are produced. As a result, antigen-antibody complexes are formed, which are more atherogenic than the drugs themselves.
Alipoproteinemia is a genetically determined disease with autosomal dominant inheritance. The disease is manifested by an increase in the tonsils with an orange coating, hepatosplenomegaly, lymphadenitis, muscle weakness, decreased reflexes, and hyposensitivity.
Hypolipoproteinemia – low blood levels of lipoproteins, often asymptomatic. The causes of the disease are:
- Heredity,
- malnutrition,
- Passive lifestyle,
- Alcoholism,
- Pathology of the digestive system,
- Endocrinopathy.
Dyslipoproteinemias are: organ or regulatory , toxigenic, basal - a study of the level of LP on an empty stomach, induced - a study of the level of LP after a meal, drugs or exercise.
Diagnostics
It is known that excess cholesterol is very harmful for the human body. But the lack of this substance can lead to dysfunction of organs and systems. The problem lies in hereditary predisposition, as well as in lifestyle and nutritional habits.
Diagnosis of dyslipoproteinemia is based on the history of the disease, complaints of patients, clinical signs - the presence of xanthoma, xanthelasma, lipoid arch of the cornea.
The main diagnostic method of dyslipoproteinemia is a blood test for lipids. Determine the coefficient of atherogenicity and the main indicators of the lipid profile - triglycerides, total cholesterol, HDL, LDL.
Lipidogram is a laboratory diagnostic method that detects lipid metabolism disorders that lead to the development of diseases of the heart and blood vessels. Lipidogram allows the doctor to assess the patient's condition, determine the risk of developing atherosclerosis of the coronary, cerebral, renal and hepatic vessels, as well as diseases of the internal organs. Blood is taken in the laboratory strictly on an empty stomach, at least 12 hours after the last meal. The day before the analysis exclude the intake of alcohol, and an hour before the study - smoking. On the eve of the analysis, it is desirable to avoid stress and emotional overstrain.
The enzymatic method for studying venous blood is the main one for determining lipids. The device fixes samples previously stained with special reagents. This diagnostic method allows you to conduct mass examinations and obtain accurate results.
It is necessary to take tests to determine the lipid spectrum for prophylactic purposes, starting from adolescence, once every 5 years. Persons over the age of 40 should do this annually. Conduct a blood test in almost every district clinic. Patients suffering from hypertension, obesity, diseases of the heart, liver and kidneys are also prescribed a lipid profile. Burdened heredity, existing risk factors, monitoring the effectiveness of treatment are indications for prescribing a lipid profile.
The results of the study may be unreliable after eating on the eve of food, smoking, stress, acute infection, during pregnancy, taking certain medications.
Diagnosis and treatment of pathology is carried out by an endocrinologist, a cardiologist, a therapist, a general practitioner, a family doctor.
Treatment
plays a huge role in the treatment of dyslipoproteinemia. Patients are advised to limit the intake of animal fats or replace them with synthetic ones, eat up to 5 times a day in small portions. The diet must be enriched with vitamins and dietary fiber. You should give up fatty and fried foods, replace meat with sea fish, eat a lot of vegetables and fruits. Restorative therapy and sufficient physical activity improve the general condition of patients.
figure: useful and harmful “diets” in terms of LP balance
Lipid-lowering therapy and antihyperlipoproteinemic drugs are designed to correct dyslipoproteinemia. They are aimed at lowering the level of cholesterol and LDL in the blood, as well as increasing the level of HDL.
Of the drugs for the treatment of hyperlipoproteinemia, patients are prescribed:
- - Lovastatin, Fluvastatin, Mevacor, Zocor, Lipitor. This group of drugs reduces the production of cholesterol by the liver, reduces the amount of intracellular cholesterol, destroys lipids and has an anti-inflammatory effect.
- Sequestrants reduce the synthesis of cholesterol and remove it from the body - Cholestyramine, Colestipol, Cholestipol, Cholestan.
- I reduce the level of triglycerides and increase the level of HDL - "Fenofibrate", "Ciprofibrat".
- B group vitamins.
Hyperlipoproteinemia requires treatment with hypolipidemic drugs "Cholesteramine", "Nicotinic acid", "Miscleron", "Clofibrate".
Treatment of the secondary form of dyslipoproteinemia is to eliminate the underlying disease. Patients with diabetes are advised to change their lifestyle, regularly take sugar-lowering drugs, as well as statins and fibrates. In severe cases, insulin therapy is required. With hypothyroidism, it is necessary to normalize the function of the thyroid gland. For this, patients undergo hormone replacement therapy.
Patients suffering from dyslipoproteinemia are recommended after the main treatment:
- Normalize body weight
- Dose physical activity,
- Limit or eliminate alcohol consumption
- Avoid stress and conflict as much as possible
- Give up smoking.
Video: lipoproteins and cholesterol - myths and reality
Video: lipoproteins in blood tests - the program “Live healthy!”
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 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 their 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.
For 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.
Upon completion of processes suction When all chylomicrons have been extracted from blood plasma, more than 95% of all plasma lipids are represented by lipoproteins. These particles are much smaller than chylomicrons, but their composition is almost similar to them, because. include triglycerides, cholesterol, phospholipids and protein. The total concentration of lipoproteins in blood plasma is approximately 700 mg per 100 ml of plasma, or 700 mg/dl.
Types of lipoproteins. In addition to chylomicrons, which are very large lipoproteins, there are four main types of lipoproteins, classified by density, determined by ultracentrifugation:
(1) very low density lipoproteins in which triglycerides are present in high concentrations and both cholesterol and phospholipids are present in moderate concentrations;
(2) intermediate density lipoproteins, from which part of the triglycerides is extracted, and therefore the representation of cholesterol and phospholipids is correspondingly increased;
(3) low density lipoproteins (LDL), obtained from the group of intermediate density lipoproteins after the extraction of almost all triglycerides, leaving a particularly high concentration of cholesterol and a moderate concentration of phospholipids;
(4) high density lipoproteins (HDL), with a high concentration of protein (about 50%), but with a much lower concentration of cholesterol and phospholipids.
Formation and function of lipoproteins. Almost all lipoproteins are formed in the liver, which is, in addition, the place where most of the cholesterol, phospholipids and triglycerides are synthesized, which then enter the blood plasma. In addition, high-density lipoproteins are formed in small amounts by intestinal epithelial cells during the absorption of fatty acids from the intestine.
Basic lipoprotein function is the transport of lipid components to tissues. Very low density lipoproteins deliver triglycerides synthesized by the liver, mainly to adipose tissue. Other lipoproteins are especially important at various stages of the transport of phospholipids and cholesterol from the liver to peripheral tissues or, conversely, from the periphery to the liver. Later in this chapter, we will take a closer look at the problems of cholesterol transport in connection with a disease such as atherosclerosis, the development of which is associated with fatty damage to the inner surface of the arterial wall.
Fats are deposited in large quantities in adipose tissue and the liver, so adipose tissue is called fat depot.
The main function of adipose tissue is to create reserves of triglycerides that can be used by the body as an energy source. A less significant function is to provide thermal insulation to the body.
Fat cells (adipocytes). Fat cells in adipose tissue are modified fibroblasts that store almost pure triglycerides in amounts ranging from 80 to 95% of the total cell volume. Triglycerides inside cells are found mainly in liquid form. If tissues are subjected to prolonged cooling, then the chains of fatty acids that make up triglycerides become either shorter after a few weeks, or the number of unsaturated bonds increases in them, reducing their melting point, which helps to preserve lipids in liquid form. This is especially important because only in liquid form can they be hydrolyzed and transported out of the cells.
fat cells synthesize very small amounts of fatty acids and triglycerides from carbohydrates. This function complements the synthesis of fats in the liver.
