Lipid metabolism is the metabolism of fats in the human body, which is complex physiological process, as well as a chain of biochemical reactions that occur in the cells of the whole body.

In order for cholesterol and triglyceride molecules to move through the bloodstream, they stick to protein molecules, which are transporters in the bloodstream.

With the help of neutral lipids, bile acids and steroid hormones are synthesized, and molecules of neutral lipids fill each cell of the membrane with energy.

By binding to low molecular density proteins, lipids are deposited on vascular membranes in the form of a lipid spot with the subsequent formation of an atherosclerotic plaque from it.

Lipoprotein composition

Lipoprotein (lipoprotein) consists of a molecule:

Esterified form of CS;
Non-esterified form of cholesterol;
Triglyceride molecules;
Protein and phospholipid molecules.

Components of proteins (proteids) in the composition of lipoprotein molecules:

Apoliprotein (apolyprotein);
Apoprotein (apoprotein).

The entire process of fat metabolism is divided into two types of metabolic processes:

Endogenous fat metabolism;
Exogenous lipid metabolism.

If lipid metabolism occurs with cholesterol molecules that enter the body with food, then this is an exogenous metabolic pathway. If the source of lipids is their synthesis by liver cells, then this is an endogenous metabolic pathway.

There are several fractions of lipoproteins, of which each fraction performs certain functions:

Chylomicron molecules (CM);
Very low molecular density lipoproteins (VLDL);
Low molecular density lipoproteins (LDL);
Medium molecular density lipoproteins (MDL);
High molecular density lipoproteins (HDL);
Triglyceride (TG) molecules.

The metabolic process between lipoprotein fractions is interconnected.

Cholesterol and triglyceride molecules are needed:

For the functioning of the hemostasis system;
To form the membranes of all cells in the body;
For the production of hormones by endocrine organs;
For the production of bile acids.

Functions of lipoprotein molecules

The structure of the lipoprotein molecule consists of a core, which includes:

Esterified cholesterol molecules;
Triglyceride molecules;
Phospholipids, which cover the core in 2 layers;
Apoliprotein molecules.

The lipoprotein molecule differs from each other in the percentage of all components.

Lipoproteins differ depending on the presence of components in the molecule:

To size;
By density;
According to its properties.

Indicators of fat metabolism and lipid fractions in the blood plasma:

lipoprotein	cholesterol content	apoliprotein molecules	molecular density unit of measurement gram per milliliter	molecular diameter
chylomicron (CM)	TG	· A-l;	less than 1,950	800,0 - 5000,0
		· A-l1;
		· A-IV;
		· B48;
		· C-l;
		· C-l1;
		· C-IIL.
residual chylomicron molecule (CM)	TG + ether CS	· B48;	less than 1.0060	more than 500.0
		· E.

VLDL	TG	· C-l;	less than 1.0060	300,0 - 800,0
		· C-l1;
		· C-IIL;
		· V-100;
		· E.
LPSP	cholesterol ester + TG	· C-l;	from 1.0060 to 1.0190	250,0 - 3500,0
		· C-l1;
		· C-IIL;
		· V-100;
		· E
LDL	TG and ether HS	V-100	from 1.0190 to 1.0630	180,0 - 280,0
HDL	TG + cholesterol ester	· A-l;	from 1.0630 to 1.210	50,0 - 120,0
		· A-l1;
		· A-IV;
		· C-l;
		· C-l1;
		· S-111.

Lipid metabolism disorder

Disorders in lipoprotein metabolism are a disruption in the process of synthesis and breakdown of fats in the human body. These abnormalities in lipid metabolism can occur in any person.

Most often the cause may be genetic predisposition the body to the accumulation of lipids, as well as unhealthy diet with high consumption of cholesterol-containing fatty foods.

Pathologies play an important role endocrine system and pathologies of the digestive tract and intestinal sections.

Causes of disorders in lipid metabolism

This pathology quite often develops as a consequence of pathological disorders in the body systems, but there is a hereditary etiology of cholesterol accumulation in the body:

Hereditary genetic chylomicronemia;
Congenital genetic hypercholesterolemia;
Hereditary genetic dys-beta-lipoproteinemia;
Combined type of hyperlipidemia;
Endogenous hyperlipidemia;
Hereditary genetic hypertriglycerinemia.

Also, disorders in lipid metabolism can be:

Primary etiology which is represented by hereditary congenital hypercholesterolemia, due to a defective gene in the child. A child can receive an abnormal gene from one parent (homozygous pathology), or from both parents (heterozygous hyperlipidemia);
Secondary etiology of disorders in fat metabolism, caused by disruptions in the endocrine system, improper functioning of liver and kidney cells;
Nutritional causes of imbalance between cholesterol fractions, comes from not proper nutrition patients when the menu is dominated by cholesterol-containing products of animal origin.

Poor nutrition

Secondary causes of disorders in lipid metabolism

Secondary hypercholesterolemia develops due to existing pathologies in the patient’s body:

Systemic atherosclerosis. This pathology can develop on the basis of primary hypercholesterolemia, as well as from poor nutrition, with a predominance of animal fats;
Addictions: nicotine and alcohol addiction. Chronic consumption affects the functionality of liver cells, which synthesize 50.0% of all cholesterol contained in the body, and chronic nicotine addiction leads to weakening of the arterial membranes, on which cholesterol plaques can be deposited;
Lipid metabolism is disrupted and diabetes mellitus;
At chronic stage liver cell failure;
With pathology of the pancreas - pancreatitis;
With hyperthyroidism;
Diseases associated with impaired functionality of endocrine organs;
When Whipple syndrome develops in the body;
With radiation sickness and malignant oncological neoplasms in organs;
Development of biliary type of cirrhosis of liver cells in stage 1;
Deviations in functionality thyroid gland;
Pathology hypothyroidism, or hyperthyroidism;
Application of many medications as self-medication, which leads not only to lipid metabolism disorders, but can also trigger irreparable processes in the body.

Factors that provoke disorders in lipid metabolism

Risk factors for disorders in fat metabolism include:

Human gender. Men are more susceptible to fat metabolism disorders. Female body protected from lipid accumulation by sex hormones in reproductive age. With the onset of menopause, women are also prone to hyperlipidemia and the development of systemic atherosclerosis and pathologies of the cardiac organ;
Patient's age. Men - after 40 - 45 years, women after 50 years of age at the time of development climacteric syndrome and menopause;
Pregnancy in a woman, an increase in the cholesterol index is due to natural biological processes in the female body;
Physical inactivity;
Poor nutrition in which maximum amount in the menu of cholesterol-containing products;
High blood pressure index - hypertension;
Excess body weight - obesity;
Cushing's pathology;
Heredity.

Medications that lead to pathological changes in lipid metabolism

Many medications provoke the occurrence of the pathology dyslipidemia. The development of this pathology can be aggravated by self-medication, when the patient does not know the exact effects of medications on the body and the interaction of drugs with each other.

Improper use and dosage lead to an increase in cholesterol molecules in the blood.

Table of medications that affect the concentration of lipoproteins in the blood plasma:

name of the drug or pharmacological group of drugs	increase in LDL index	increase in triglyceride index	decrease in HDL index
thiazide-type diuretics	+
drug Cyclosporine	+
medication Amiodarone	+
The drug Rosiglitazone	+
bile sequestrants		+
group of drugs inhibiting proteinase		+
medicines retinoids		+
group of glucocorticoids		+
group of anabolic steroid medications		+
drug Sirolimus		+
beta blockers		+	+
progestin group			+
androgen group			+

When using hormone replacement therapy, the hormone estrogen and the hormone progesterone, which are part of medications, reduce HDL molecules in the blood.

Oral contraceptive medications also reduce high molecular weight cholesterol in the blood.

Other drugs with long-term therapy lead to changes in lipid metabolism and can also disrupt the functionality of liver cells.

Signs of changes in lipid metabolism

Symptoms of the development of hypercholesterolemia of primary etiology (genetic) and secondary etiology (acquired) cause a large number of changes in the patient’s body.

Many symptoms can only be identified through diagnostic study instrumental and laboratory techniques, but there are also symptoms that can be detected visually and when using the palpation method:

Xanthomas form on the patient’s body;
Formation of xanthelasmas on the eyelids and on the skin;
Xanthomas on tendons and joints;
The appearance of cholesterol deposits in the corners of the eye incisions;
Body weight increases;
There is an enlargement of the spleen, as well as the liver organ;
Diagnosed obvious signs development of nephrosis;
Generalized symptoms of endocrine system pathology are formed.

This symptomatology indicates a violation of lipid metabolism and an increase in the cholesterol index in the blood.

When there is a change in lipid metabolism towards a decrease in lipids in the blood plasma, the following symptoms are pronounced:

Body weight and volume decrease, which can lead to complete exhaustion of the body - anorexia;
Hair loss from the scalp;
Separation and brittleness of nails;
Eczema and ulcers on the skin;
Inflammatory processes on the skin;
Dry skin and exfoliation of the epidermis;
Pathology nephrosis;
Disorders of the menstrual cycle in women;
Female infertility.

Symptoms of changes in lipid metabolism are the same in children's body and in the adult body.

Children more often show external signs of an increase in the cholesterol index in the blood, or a decrease in lipid concentrations, and in an adult body, external signs appear when the pathology progresses.

Diagnostics

To establish the correct diagnosis, the doctor must examine the patient and also refer the patient for laboratory diagnostics of blood composition. Only in the aggregate of all the research results can an accurate diagnosis of changes in lipid metabolism be made.

The primary diagnostic method is carried out by the doctor at the patient’s first appointment:

Visual examination of the patient;
Studying the pathology of not only the patient himself, but also genetic relatives to identify familial hereditary hypercholesterolemia;
Anamnesis collection. Special attention pays attention to the patient’s nutrition, as well as lifestyle and addictions;
The use of palpation of the anterior wall of the peritoneum, which will help identify the pathology of hepatosplenomegaly;
The doctor measures the blood pressure index;
A complete survey of the patient about the onset of the development of pathology in order to be able to establish the onset of changes in lipid metabolism.

Laboratory diagnosis of disorders in lipid metabolism is carried out using the following method:

General analysis of blood composition;
Biochemistry of plasma blood composition;
General urine analysis;
Laboratory blood test with metol lipid spectrum- lipograms;
Immunological analysis of blood composition;
Blood to identify the index of hormones in the body;
Study of genetic detection of defective and abnormal genes.

Methods instrumental diagnostics for disorders of fat metabolism:

Ultrasound ( ultrasonography) liver and kidney cells;
CT ( CT scan) internal organs, which are involved in lipid metabolism;
MRI (magnetic resonance imaging) of internal organs and the blood flow system.

How to restore and improve cholesterol metabolism?

Correcting fat metabolism disorders begins with a review of lifestyle and nutrition.

The first step after making a diagnosis is to immediately:

Give up existing bad habits;
Increase your activity, you can start riding a bike, or go to the pool. A 20-30 minute session on an exercise bike will do, but riding a bike takes longer. fresh air, preferable;
Constant control of body weight and the fight against obesity;
Diet food.

A diet for liposynthesis disorders can:

Restore lipid and carbohydrate metabolism in the patient;
Improve the functioning of the heart organ;
Restore blood microcirculation in the cerebral vessels;
Normalization of metabolism of the whole body;
Reduce bad cholesterol levels to 20.0%;
Prevent the formation of cholesterol plaques in the main arteries.

Restoring lipid metabolism with nutrition

Dietary nutrition for disorders of the metabolism of lipids and lipid-like compounds in the blood is initially the prevention of the development of atherosclerosis and diseases of the heart organ.

Diet not only acts as an independent part non-drug therapy, but also as a component of a complex of drug treatment with drugs.

The principle of proper nutrition to normalize fat metabolism:

Limit consumption of cholesterol-containing foods. Eliminate from the diet foods containing animal fat - red meats, fatty dairy products, eggs;
Meals in small portions, but not less than 5 - 6 times a day;
Enter in daily diet foods that are rich in fiber are fresh fruits and berries, fresh and boiled and stewed vegetables, as well as cereals and legumes. Fresh vegetables and fruits will fill the body with a whole complex of vitamins;
Eat sea fish up to 4 times a week;
Use daily in cooking vegetable oils, which contain Omega-3 polyunsaturated fatty acids - olive, sesame and flaxseed oil;
Eat only lean meats, and cook and eat poultry without skin;
Fermented milk products must have 0% fat content;
Introduce nuts and seeds into your daily menu;
Increased drinking. Drink at least 2000.0 milliliters per day clean water.

Drink at least 2 liters of clean water

Correcting impaired lipid metabolism with the help of medications gives the best result in normalizing the total cholesterol index in the blood, as well as restoring the balance of lipoprotein fractions.

Drugs used to restore lipoprotein metabolism:

group of drugs	LDL molecules	triglyceride molecules	HDL molecules	therapeutic effect
statin group	decrease 20.0% - 55.0%	decrease 15.0% - 35.0%	increase 3.0% - 15.0%	shows a good therapeutic effect in the treatment of atherosclerosis, as well as in primary and secondary prevention of development cerebral stroke and myocardial infarction.
fibrate group	decrease 5.0% - 20.0%	reduction 20.0% - 50.0%	increase 5.0% - 20.0%	enhancing the transport properties of HDL molecules to deliver cholesterol back to liver cells for its utilization. Fibrates have anti-inflammatory properties.
bile sequestrants	decrease 10.0% - 25.0%	decrease 1.0% - 10.0%	increase 3.0% - 5.0%	good medicinal effect with a significant increase in triglycerides in the blood. There are disadvantages in the tolerability of the drug by the digestive tract.
drug Niacin	decrease 15.0% - 25.0%	reduction 20.0% - 50.0%	increase 15.0% 35.0%	most effective drug by increasing the HDL index, and also effectively reduces the lipoprotein A index.
drug Niacin	decrease 15.0% - 25.0%	reduction 20.0% - 50.0%	increase 15.0% 35.0%	The drug has proven itself in the prevention and treatment of atherosclerosis with positive dynamics of therapy.
drug Ezetimibe	decrease 15.0% - 20.0%	decrease 1.0% - 10.0%	increase 1.0% - 5.0%	has a therapeutic effect when used with drugs of the statin group. The drug prevents the absorption of lipid molecules from the intestines.
fish oil - Omega-3	increase 3.0% - 5.0;	decrease 30.0% - 40.0%	no changes appear	These drugs are used in the treatment of hypertriglyceridemia and hypercholesterolemia.

Using folk remedies

Lipid metabolism disorders can be treated with medicinal plants and herbs only after consultation with your doctor.

Effective plants in restoring lipoprotein metabolism:

Plantain leaves and roots;
Immortelle flowers;
Horsetail leaves;
Chamomile and calendula inflorescences;
Leaves of knotweed and St. John's wort;
Hawthorn leaves and fruits;
Leaves and fruits of strawberries and viburnum plants;
Dandelion roots and leaves.

Traditional medicine recipes:

Take 5 spoons of strawberry flowers and steam with 1000.0 milliliters of boiling water. Leave for 2 hours. Take 3 times a day, 70.0 - 100.0 milligrams. This infusion restores the functioning of liver and pancreas cells;
Every morning and every evening, take 1 teaspoon of crushed flax seeds. You need to drink 100.0 - 150.0 milliliters of water or skim milk;

Life forecast

The prognosis for life is individual for each patient, because the failure of lipid metabolism in each has its own etiology.

If a malfunction in metabolic processes in the body is diagnosed in a timely manner, then the prognosis is favorable.

>> Digestion of fats, regulation of metabolism

Metabolism of fats (lipids) in the human body

Fat (lipid) metabolism in the human body consists of three stages

1. Digestion and absorption of fats in the stomach and intestines

2. Intermediate metabolism of fats in the body

3. Excretion of fats and their metabolic products from the body.

Fats are part of a large group organic compounds- lipids, therefore the concepts of “fat metabolism” and “lipid metabolism” are synonymous.

The adult human body receives about 70 grams of animal fats per day and plant origin. Fat breakdown does not occur in the oral cavity, since saliva does not contain the corresponding enzymes. Partial breakdown of fats into components (glycerol, fatty acids) begins in the stomach, but this process is slow for the following reasons:

1. in gastric juice in an adult, the activity of the enzyme (lipase) for the breakdown of fats is very low,

2. acidic - alkaline balance in the stomach is not optimal for the action of this enzyme,

3. in the stomach there are no conditions for emulsification (splitting into small droplets) of fats, and lipase actively breaks down fats only in the composition of a fat emulsion.

Therefore, in an adult most of fat passes through the stomach without significant changes.

Unlike adults, in children the breakdown of fats in the stomach occurs much more actively.

The main part of dietary lipids undergoes breakdown in the upper part of the small intestine, under the influence of pancreatic juice.

Successful breakdown of fats is possible if they first break down into small droplets. This occurs under the influence of bile acids entering the duodenum with bile. As a result of emulsification, the surface of fats sharply increases, which facilitates their interaction with lipase.

Absorption of fats and other lipids occurs in small intestine. Together with the products of fat breakdown, fat-soluble acids (A, D, E, K) enter the body.

The synthesis of fats specific to a given organism occurs in the cells of the intestinal wall. Subsequently, the newly created fats enter the lymphatic system, and then into the blood. The maximum fat content in the blood plasma occurs between 4 and 6 hours after eating a fatty meal. After 10 - 12 hours, the fat concentration returns to normal.

The liver takes an active part in fat metabolism. In the liver, some of the newly formed fats are oxidized to form the energy necessary for the body’s functioning. The other part of the fats is converted into a form convenient for transportation and enters the blood. Thus, from 25 to 50 grams of fat are transferred per day. Fats that the body does not immediately use are carried through the bloodstream into fat cells, where they are stored as reserves. These compounds can be used during fasting, exercise, and so on.

Fats are an important source of energy for our body. During short-term and sudden loads, the energy of glycogen, which is located in the muscles, is first used. If the load on the body does not stop, then the breakdown of fats begins.

From this you need to draw a conclusion if you want to get rid of extra pounds with the help of physical activity, it is necessary that these loads be long enough for at least 30 - 40 minutes.

Fat metabolism is very closely related to carbohydrate metabolism. With an excess of carbohydrates in the body, fat metabolism slows down, and work goes only in the direction of synthesizing new fats and storing them in reserve. If there is a lack of carbohydrates in food, on the contrary, the breakdown of fats from the fat reserve is activated. From this we can conclude that nutrition for weight loss should limit (within reasonable limits) not only the consumption of fats, but also carbohydrates.

Most of the fats we eat are used by our body or stored in reserve. Under normal conditions, only 5% of fats are excreted from our body, this is done with the help of the sebaceous and sweat glands.

Regulation of fat metabolism

Regulation of fat metabolism in the body occurs under the guidance of the central nervous system. Our emotions have a very strong influence on fat metabolism. Under the influence of various strong emotions, substances enter the bloodstream that activate or slow down fat metabolism in the body. For these reasons, one must eat in a calm state of consciousness.

Disorders of fat metabolism can occur with a regular lack of vitamins A and B in food.

The physicochemical properties of fat in the human body depend on the type of fat supplied with food. For example, if a person’s main source of fat is vegetable oils (corn, olive, sunflower), then the fat in the body will have a more liquid consistency. If animal fats (lamb, pork fat) predominate in human food, then fats more similar to animal fat (hard consistency with high temperature melting). There is experimental confirmation of this fact.

How to remove trans fatty acids from the body

One of the most important tasks that modern people face is how to cleanse their own body of toxins and poisons that have accumulated “thanks to” poor quality daily nutrition. A significant role in polluting the body is played by trans fats, which are abundantly supplied with daily food and over time greatly inhibit the functioning of internal organs.

Basically, trans fatty acids are eliminated from the body due to the ability of cells to renew. Some cells die and new ones appear in their place. If there are cells in the body whose membranes consist of trans-fatty acids, then after they die, new cells may appear in their place, the membranes of which consist of high-quality fatty acids. This happens if a person excludes foods containing trans fatty acids from the diet.

To ensure that as little trans fatty acids as possible penetrate cell membranes, you need to increase the amount of Omega-3 fatty acids you consume daily. By consuming foods containing such oils and fats, you can ensure that the membranes of nerve cells have the correct structure, which will have a positive effect on the functioning of the brain and nervous system.

We must remember that during heat treatment, fats can decompose to form irritating and harmful substances. Overheating fats reduces their nutritional and biological value.

Additional articles with useful information

Why do humans need fats?

A lack of fat in food significantly undermines human health, and if it is present in the diet healthy fats, then a person makes his life significantly easier by increasing physical and mental performance.

Description of the types of obesity and methods of treating this disease

Obesity has recently become increasingly widespread among the world's population, and this disease requires long-term and systemic treatment.

Lipid metabolism disorder is a disorder in the process of production and breakdown of fats in the body, which occurs in the liver and adipose tissue. Any person can have such a disorder. The most common cause of the development of this disease is genetic predisposition and poor nutrition. In addition, gastroenterological diseases play an important role in the formation.

This disorder has quite specific symptoms, namely enlargement of the liver and spleen, rapid weight gain and the formation of xanthoma on the surface skin.

The correct diagnosis can be made based on the data laboratory research, which will show changes in blood composition, as well as using information obtained during an objective physical examination.

It is customary to treat such a metabolic disorder using conservative methods, among which the main place is given to diet.

Etiology

Such a disease very often develops during the course of various pathological processes. Lipids are fats that are synthesized by the liver or enter the human body with food. A similar process performs a large number of important functions, and any failures in it can lead to the development of quite large quantity ailments.

The causes of the disorder can be either primary or secondary. The first category of predisposing factors consists of hereditary genetic sources, in which single or multiple anomalies of certain genes responsible for the production and utilization of lipids occur. Provocateurs of a secondary nature are caused by an irrational lifestyle and the course of a number of pathologies.

Thus, the second group of reasons can be represented:

In addition, clinicians identify several groups of risk factors that are most susceptible to disorders of fat metabolism. These include:

gender - in the vast majority of cases, such pathology is diagnosed in males;
age category - this includes postmenopausal women;
period of bearing a child;
maintaining a sedentary and unhealthy lifestyle;
poor nutrition;
presence of excess body weight;
liver or kidney pathologies previously diagnosed in a person;
course or endocrine diseases;
hereditary factors.

Classification

In the medical field, there are several varieties of this disease, the first of which divides it depending on the mechanism of development:

primary or congenital disorder of lipid metabolism- this means that the pathology is not associated with the course of any disease, but is hereditary in nature. The defective gene can be received from one parent, less often from two;
secondary- lipid metabolism disorders often develop due to endocrine diseases, as well as diseases of the gastrointestinal tract, liver or kidneys;
nutritional- is formed due to the fact that a person eats a large amount of animal fats.

Based on the level of which lipids are elevated, there are the following forms of lipid metabolism disorders:

pure or isolated hypercholesterolemia- characterized by increased cholesterol levels in the blood;
mixed or combined hyperlipidemia- at the same time during laboratory diagnostics elevated levels of both cholesterol and triglycerides are detected.

It is worth highlighting the rarest variety - hypocholesterolemia. Its development is promoted by liver damage.

Modern research methods have made it possible to identify the following types of disease progression:

hereditary hyperchylomicronemia;
congenital hypercholesterolemia;
hereditary dys-beta lipoproteinemia;
combined hyperlipidemia;
endogenous hyperlipidemia;
hereditary hypertriglyceridemia.

Symptoms

Secondary and hereditary disorders of lipid metabolism lead to a large number of changes in the human body, which is why the disease has many both external and internal clinical signs, the presence of which can only be detected after laboratory diagnostic examinations.

The disease has the following most pronounced symptoms:

the formation of xanthomas and any localization on the skin, as well as on the tendons. The first group of neoplasms are nodules containing cholesterol and affecting the skin of the feet and palms, back and chest, shoulders and face. The second category also consists of cholesterol, but has a yellow tint and occurs on other areas of the skin;
the appearance of fatty deposits in the corners of the eyes;
increased body mass index;
- this is a condition in which the liver and spleen are enlarged;
the occurrence of manifestations characteristic of nephrosis and endocrine diseases;
increased blood tone.

The above clinical signs of lipid metabolism disorders appear when lipid levels increase. In cases of their deficiency, symptoms may include:

loss of body weight, up to extreme exhaustion;
hair loss and splitting of nail plates;
the appearance of other inflammatory skin lesions;
nephrosis;
menstrual irregularities and reproductive functions among women.

It is advisable to apply all of the above symptoms to both adults and children.

Diagnostics

To make a correct diagnosis, the clinician needs to review the data wide range laboratory tests, but before prescribing them, the doctor must independently perform several manipulations.

Thus, primary diagnosis is aimed at:

studying the medical history, not only of the patient, but also of his immediate relatives, because the pathology can be hereditary;
collecting a person’s life history - this should include information regarding lifestyle and nutrition;
performing a thorough physical examination - to assess the condition of the skin, palpation of the anterior wall of the abdominal cavity, which will indicate hepatosplenomegaly, and also to measure blood pressure;
a detailed interview with the patient is necessary to establish the first time of appearance and severity of symptoms.

Laboratory diagnosis of impaired lipid metabolism includes:

general clinical blood test;
blood biochemistry;
general analysis urine;
lipid profile - will indicate the content of triglycerides, “good” and “bad” cholesterol, as well as the atherogenicity coefficient;
immunological blood test;
blood test for hormones;
genetic research aimed at identifying defective genes.

Instrumental diagnostics in the form of CT and ultrasound, MRI and radiography are indicated in cases where the clinician suspects the development of complications.

Treatment

Lipid metabolism disorders can be eliminated using conservative methods of therapy, namely:

non-drug methods;
reception medicines;
maintaining a gentle diet;
using traditional medicine recipes.

Non-drug treatment methods include:

normalization of body weight;
performance physical exercise- volumes and load conditions are selected according to individually for each patient;
giving up harmful addictions.

The diet for such a metabolic disorder is based on the following rules:

enrichment of the menu with vitamins and dietary fiber;
minimizing the consumption of animal fats;
eating plenty of fiber-rich vegetables and fruits;
replacing fatty meats with fatty fish;
using rapeseed, flaxseed, nut or hemp oil for seasoning dishes.

Treatment with medications is aimed at taking:

statins;
inhibitors of cholesterol absorption in the intestine - to prevent the absorption of such a substance;
Bile acid sequestrants are a group of medications aimed at binding bile acids;
Omega-3 polyunsaturated fatty acids - to reduce triglyceride levels.

In addition, therapy is allowed folk remedies, but only after prior consultation with a clinician. The most effective are decoctions prepared on the basis of:

plantain and horsetail;
chamomile and knotweed;
hawthorn and St. John's wort;
birch buds and immortelle;
viburnum and strawberry leaves;
fireweed and yarrow;
dandelion roots and leaves.

If necessary, extracorporeal therapy methods are used, which involve changing the composition of the blood outside the patient’s body. For this, special devices are used. This treatment is allowed for pregnant women and children whose weight exceeds twenty kilograms. Most often used:

immunosorption of lipoproteins;
cascade plasma filtration;
plasma sorption;
hemosorption.

Possible complications

Impaired lipid metabolism in metabolic syndrome can lead to the following consequences:

atherosclerosis, which can affect the vessels of the heart and brain, arteries of the intestines and kidneys, lower extremities and aorta;
stenosis of the lumen of blood vessels;
formation of blood clots and emboli;
vessel rupture.

Prevention and prognosis

To reduce the likelihood of developing lipid metabolism disorders, there are no specific preventive measures, which is why people are advised to adhere to general recommendations:

maintaining a healthy and active lifestyle;
preventing development;
proper and balanced nutrition - it is best to follow a diet low in animal fats and salt. Food should be enriched with fiber and vitamins;
elimination of emotional stress;
timely fight against arterial hypertension and other ailments that lead to secondary metabolic disorders;
Regularly undergoing a full examination at a medical facility.

The prognosis will be individual for each patient, since it depends on several factors - the level of lipids in the blood, the rate of development of atherosclerotic processes, and the localization of atherosclerosis. However, the outcome is often favorable, and complications develop quite rarely.

Is everything in the article correct from a medical point of view?

Answer only if you have proven medical knowledge

Human lipids include compounds that vary significantly in both structure and function in a living cell. The most important groups of lipids in terms of function are:

1) Triacylglycerols (TAG) – important source energy. Among nutrients, they are the most caloric. About 35% of a person's daily energy requirement is covered by TAG. In some organs, such as the heart and liver, over half of the required energy is supplied by TAG.

2) Phospholipids and glycolipids are the most important components cell membranes. At the same time, some phospholipids perform special functions: a) dipalmitoyllecithin is the main element of lung surfactant. Its absence in premature infants can lead to respiratory disorders; b) Phosphatidylinositol is a precursor of secondary hormonal messengers; c) platelet-activating factor, which is an alkylphospholipid in nature, plays an important role in the pathogenesis of bronchial asthma, coronary artery disease and other diseases.

3) Steroids. Cholesterol is part of cell membranes and also serves as a precursor to bile acids, steroid hormones, and vitamin D 3 .

4) Prostaglandins and leukotrienes are derivatives of arachidonic acid that perform regulatory functions in the body.

Fatty acid metabolism

The source of fatty acids for the body are food lipids, as well as the synthesis of fatty acids from carbohydrates. The use of fatty acids occurs in three directions: 1) oxidation to CO 2 and H 2 O with the formation of energy, 2) deposition in adipose tissue in the form of TAG, 3) synthesis of complex lipids.

All transformations of free fatty acids in cells begin with the formation of acyl-CoA. This reaction is catalyzed by acyl-CoA synthetases localized on the outer mitochondrial membrane:

R-COOH+ CoA + ATP → acyl-CoA + AMP + H 4 P 2 O 7

Taking this circumstance into account, the main pathways for the transformation of fatty acids can be presented as follows:

Oxidation of fatty acids with an even number of carbon atoms

Fatty acid oxidation occurs in the mitochondrial matrix. However, acyl-CoA formed in the cytoplasm is unable to penetrate the inner mitochondrial membrane. Therefore, the transport of acyl groups is carried out using a special carrier - carnitine (considered as a vitamin-like substance) and two enzymes - carnitine acyltransferase I (CAT 1) and CAT 2. First, under the influence of CAT 1, acyl groups are transferred from acyl-CoA to carnitine with the formation acyl-carnitine complex:

Acyl-CoA + carnitine → acyl-carnitine + CoA

The resulting acyl-carnitine penetrates through the inner mitochondrial membrane and on the inner side of the inner mitochondrial membrane, with the participation of the enzyme CAT 2, the acyl group is transferred from acyl-carnitine to intramitochondrial CoA with the formation of acyl-CoA:

acyl-carnitine + CoA → Acyl-CoA + carnitine

The released carnitine enters a new cycle of transport of acyl groups, and fatty acid residues undergo oxidation in a cycle called β-oxidation of fatty acids.

The process of fatty acid oxidation involves the sequential elimination of two-carbon fragments from the carboxyl end of the fatty acid. Each two-carbon fragment is cleaved as a result of a cycle of 4 enzymatic reactions:

Fate of the resulting products: acetyl-CoA enters the cycle citric acid, FADH 2 and NADH·H + transfer protons and electrons to the respiratory chain, and the resulting acyl-CoA enters a new oxidation cycle, consisting of the same 4 reactions. Repeating this process many times leads to the complete breakdown of the fatty acid to acetyl-CoA.

Calculation of the energy value of fatty acids

using palmitic acid as an example(From 16).

The oxidation of palmitic acid to form 8 molecules of acetyl-CoA requires 7 oxidation cycles. The number of oxidation cycles is calculated by the formula:

n = C/2 – 1,

where C is the number of carbon atoms.

Thus, as a result of complete oxidation of palmitic acid, 8 molecules of acetyl-CoA and 7 molecules of FADH 2 and NADH·H + are formed. Each molecule of acetyl-CoA produces 12 molecules of ATP, FADH 2 - 2 molecules of ATP and NADH·H + - 3 molecules of ATP. Let’s sum it up and get: 8 12 + 7 (2 + 3) = 96 + 35 = 131. After subtracting 2 ATP molecules spent at the fatty acid activation stage, we get a total output of 129 ATP molecules.

Importance of fatty acid oxidation

The utilization of fatty acids by β-oxidation occurs in many tissues. The role of this source of energy is especially important in the cardiac muscle and skeletal muscles during prolonged physical work.

Oxidation of fatty acids with an odd number of carbon atoms

Fatty acids with an odd number of carbon atoms enter the human body in small quantities with plant foods. They are oxidized in the same sequence as fatty acids with an even number of “C” atoms, i.e. by removing two-carbon moieties from the carboxyl end of a fatty acid. In this case, at the final stage of β-oxidation, propionyl-CoA is formed. In addition, propionyl-CoA is formed during the catabolism of amino acids with a branched side radical (valine, isoleucine, threonine). Propionyl-CoA has its own metabolic pathway:

First, with the participation of propionyl-CoA carboxylase, carboxylation of propionyl-CoA occurs to form methylmalonyl-CoA. Methylmalonyl-CoA is then converted by methylmalonyl-CoA mutase to succinyl-CoA, a metabolite of the citric acid cycle. The coenzyme of methylmalonyl-CoA mutase is deoxyadenosylcobalamin, one of the coenzyme forms of vitamin B12. With a lack of vitamin B 12, this reaction slows down and large amounts of propionic and methylmalonic acids are excreted in the urine.

Synthesis and use of ketone bodies

Acetyl-CoA is included in the citrate cycle under conditions when the oxidation of carbohydrates and lipids is balanced, because the incorporation of acetyl-CoA, formed during the oxidation of fatty acids, into CLA depends on the availability of oxaloacetate, which is mainly a product of carbohydrate metabolism.

Under conditions where lipid breakdown predominates (diabetes mellitus, fasting, low-carbohydrate diet), the resulting acetyl-CoA enters the pathway of ketone body synthesis.

Free acetoacetate is reduced in a reversible reaction to β-hydroxybutyrate or decarboxylated spontaneously or enzymatically to acetone.

Acetone is not utilized by the body as a source of energy and is excreted from the body through urine, sweat and exhaled air. Acetoacetate and β-hydroxybutyrate normally act as fuel and are important sources of energy.

Due to the absence of 3-ketoacyl-CoA transferase in the liver, the liver itself is not able to use acetoacetate as an energy source, supplying it to other organs. Thus, acetoacetate can be considered as a water-soluble transport form of acetyl residues.

Biosynthesis of fatty acids

The synthesis of fatty acids has a number of features:

Unlike oxidation, synthesis is localized in the cytosol.

The immediate precursor of the seven (out of eight) two-carbon fragments of the palmitic acid molecule is malonyl-CoA, formed from acetyl-CoA.

Acetyl-CoA is used directly as a primer in synthesis reactions.

To restore the intermediate processes of fatty acid synthesis, NADPHH + is used.

All stages of fatty acid synthesis from malonyl-CoA are a cyclic process that occurs on the surface of fatty acid synthase or palmitate synthase, since the main fatty acid in human lipids is palmitic acid.

The formation of malonyl-CoA from acetyl-CoA occurs in the cytosol. Acetyl-CoA, in turn, is formed from citrate, which comes from mitochondria and is broken down in the cytoplasm by the enzyme ATP-citrate lyase:

Citrate + ATP + CoA → acetyl-CoA + oxaloacetate + ADP + H 3 PO 4

The resulting acetyl-CoA undergoes carboxylation using the enzyme acetyl-CoA carboxylase:

A
cetyl-CoA carboxylase is a regulatory enzyme. The reaction catalyzed by this enzyme is the rate-limiting step that determines the rate of the entire process of fatty acid biosynthesis. Acetyl-CoA carboxylase is activated by citrate and inhibited by long-chain acyl-CoA.

Subsequent reactions take place on the surface of palmitate synthase. Mammalian palmitate synthase is a multifunctional enzyme consisting of 2 identical polypeptide chains, each of which has 7 active sites and an acyl transfer protein that transfers the growing fatty acid chain from one active site to another. Each of the proteins has 2 binding centers containing SH groups. Therefore, this complex is briefly denoted:

The central place in each of the proteins is occupied by the acyl transfer protein (ATP), which contains phosphorylated pantothenic acid (phosphopantetheine). Phosphopanthetheine has an –SH group at the end. In the first step, the acetyl residue is transferred to the SH group of cysteine, and the malonyl residue is transferred to the SH group of 4'-phosphopantetheine palmitate synthase (acyltransferase activity) (reactions 1 and 2).

Next, in reaction 3, the acetyl residue is transferred to the place of the carboxyl group of the malonyl residue; the carboxyl group is split off in the form of CO 2 . Then, the reduction of the 3-carbonyl group (reaction 4), elimination of water with the formation of a double bond between -(2) and -(3) carbon atoms (reaction 5), and reduction of the double bond (reaction 6) occur sequentially. The result is a four-carbon acid residue linked to the enzyme via pantothenic acid (butyryl-E). Next, the new malonyl-CoA molecule interacts with the SH group of phosphopantetheine, and the saturated acyl residue is transferred to the free SH group of cysteine.

1. Transfer of acetyl from acetyl-CoA to synthase.

2. transfer of malonyl from malonyl-CoA to synthase.

3. stage of condensation of acetyl with malonyl and decarboxylation of the resulting product.

4. first reduction reaction

5. dehydration reaction

6. second reduction reaction

After this, the butyryl group is transferred from one HS group to another, and a new malonyl residue is placed in the vacated space. The synthesis cycle is repeated. After 7 such cycles, the final product is formed - palmitic acid. The chain extension process ends here and then, under the action of a hydrolytic enzyme, the palmitic acid molecule is cleaved from the synthase molecule.

Synthesis of unsaturated fatty acids

The formation of a double bond in a fatty acid molecule occurs as a result of an oxidation reaction catalyzed by acyl-CoA desaturase. The reaction proceeds according to the scheme:

palmitoyl-CoA + NADPH H + + O 2 → palmitoleyl-CoA + NADP + + H 2 O

In human tissues, a double bond at the Δ 9 position of a fatty acid molecule is easily formed, whereas the formation of a double bond between the Δ 9 double bond and the methyl end of the fatty acid is impossible. Therefore, a person is not able to synthesize linoleic acid (C 18 Δ 9.12) and α-linolenic acid (C 18 Δ 9.12.15). These polyunsaturated fatty acids are used in the body as precursors in the synthesis of arachidonic acid (C 20 Δ 5,8,11,14), so they must be supplied with food. These polyunsaturated fatty acids are called essential fatty acids. Arachidonic acid, in turn, serves as a precursor in the synthesis of prostaglandins, leukotrienes and thromboxanes.

Regulation of oxidation and synthesis of fatty acids in the liver

Enzyme systems for both synthesis and breakdown of fatty acids are highly active in the liver. However, these processes are separated in space and time. Oxidation of fatty acids occurs in mitochondria, while synthesis occurs in the cytosol of the cell. Separation in time is achieved through the action of regulatory mechanisms consisting of allosteric activation and inhibition of enzymes.

The highest rate of synthesis of fatty acids and fats is observed after eating carbohydrate foods. Under these conditions, a large amount of glucose enters the liver cells; glucose (during glycolysis) is oxidized to pyruvate, which is often converted into oxaloacetate:

pyruvate + CO 2 oxaloacetate

pyruvate acetyl-CoA

Upon entering the CLC, these compounds are converted into citrate. Excess citrate enters the cell cytosol, where it activates acetyl-CoA carboxylase, a key enzyme in the synthesis of fatty acids. On the other hand, citrate is a precursor of cytoplasmic acetyl-CoA. This leads to an increase in the concentration of malonyl-CoA and the onset of fatty acid synthesis. Malonyl-CoA inhibits carnitine acyltransferase I, as a result of which the transport of acyl groups into mitochondria stops, and therefore their oxidation stops. Thus, when the synthesis of fatty acids is turned on, their breakdown is automatically turned off. On the contrary, during the period when the concentration of oxaloacetate decreases, the flow of citrate into the cytosol weakens and the synthesis of fatty acids ceases. A decrease in the concentration of malonyl-CoA opens the way for acyl residues into the mitochondria, where their oxidation begins. This mechanism ensures the primary use of carbohydrates: the liver stores or even replenishes the body's fat reserves when there are carbohydrates, and only as they are depleted does the use of fat begin.

Triacylglycerol metabolism

Natural fats are a mixture of TAGs that differ in fatty acid composition. Human TAG contains many unsaturated fatty acids, so human fat has low temperature melting (10–15 o C) and is in the cells in a liquid state.

Digestion of fats

Fats are one of the main groups nutrients person. The daily need for them is 50-100 g.

In an adult, conditions for the digestion of lipids are available only in the upper parts of the intestine, where there is a suitable environment and where the enzyme - pancreatic lipase and emulsifiers - bile acids arrive. Pancreatic lipase enters the intestine in a reactive form - in the form of prolipase. Activation occurs with the participation of bile acids and another protein of pancreatic juice - colipase. The latter joins prolipase in a molar ratio of 2: 1. As a result, lipase becomes active and resistant to trypsin.

Active lipase catalyzes the hydrolysis of ester bonds in the - and  1-positions, resulting in the formation of -MAG and the release of two fatty acids. In addition to lipase, pancreatic juice contains monoglyceride isomerase, an enzyme that catalyzes the intramolecular transfer of acyl from the α-position of MAG to the α-position. And the ester bond in the α-position is sensitive to the action of pancreatic lipase.

Absorption of digestion products

The main part of TAG is absorbed after their cleavage by lipase into β-MAG and fatty acids. Absorption occurs with the participation of bile acids, which form micelles with MAG and fatty acids that penetrate the cells of the intestinal mucosa. From here, bile acids enter the blood, and with it into the liver and re-participate in the formation of bile. The hepatoenteric circulation of bile acids from the liver to the intestine and back is extremely important, ensuring the absorption of large quantities of MAG and fatty acids (up to 100 or more g/day) with a relatively small total stock of bile acids (2.8-3.5 g). Normally, only a small part of bile acids (up to 0.5 g/day) is not absorbed and is excreted in feces. If bile formation or excretion of bile is impaired, the conditions for the digestion of fats and absorption of hydrolysis products worsen, and a significant part of them is excreted in the feces. This condition is called steatorrhea. At the same time, fat-soluble vitamins are also not absorbed, which leads to the development of hypovitaminosis.

Resynthesis of fats in intestinal cells

Most of the products of lipid digestion in intestinal cells are converted back into TAG. Fatty acids form acyl-CoA, then acyl residues are transferred to MAG with the participation of acyltransferases.

Formation of fats from carbohydrates

Some of the carbohydrates that come from food are converted into fats in the body. Glucose serves as a source of acetyl-CoA, from which fatty acids are synthesized. Necessary for reduction reactions, NADPHH + is formed during the oxidation of glucose in the pentose phosphate pathway, and glycerol-3-phosphate is obtained by the reduction of dihydroxyacetone phosphate, a metabolite of glycolysis.

Due to the absence of glycerol kinase in adipose tissue, this pathway for the formation of glycerol-3-phosphate is the only one in adipocytes. Thus, all the components necessary for the synthesis of fats are formed from glucose. The synthesis of TAG from glycerol-3-phosphate and acyl-CoA proceeds according to the following scheme:

The synthesis of fats from carbohydrates occurs most actively in the liver and less actively in adipose tissue.

How is fat formed in the human body?

The human body can form lipids or triglycerides not only from fats coming from food, but also from carbohydrates and proteins. Fats from incoming food enter the gastrointestinal tract, are absorbed into small intestine, undergo a transformation process and are broken down into fatty acids and glycerol. There are also internal, endogenous fats that are synthesized in the liver. Fatty acids are a source of large amounts of energy, being a kind of body “fuel”.

They are absorbed into the blood and, with the help of special transport forms - lipoproteins, chylomicrons, are carried to various bodies and fabrics. Fatty acids can again be used for the synthesis of triglycerides and fat, and if they are in excess, they can be stored in the liver and in adipose tissue cells - adipocytes. It is adipocytes with a large supply of triglycerides that create discomfort for a person and are manifested by excess deposits of subcutaneous fat and excess weight. Fat deposits can also be formed from carbohydrates.

Glucose and fructose entering the blood with the help of the hormone insulin can be deposited in the form of triglycerides in the liver and cells. Proteins supplied with food are also capable of being transformed into triglycerides through a cascade of transformations: broken down proteins into amino acids are absorbed into the blood, penetrate into the liver, are converted into glucose and, under the action of insulin, become triglycerides stored in adipocytes. This is a very simplified way to imagine the process of lipid formation in the human body.

2 Functions of lipids in the body

The role of fats in the human body is difficult to overestimate. They are:

the main energy source in the body;
building material for cell membranes, organelles, a number of hormones and enzymes;
a protective “cushion” for internal organs.

Fat cells carry out thermoregulation, increase the body's resistance to infection, secrete hormone-like substances - cytokines, and also regulate metabolic processes.

3 How are fats used?

Triglycerides stored “in reserve” can leave adipocytes and be used for cell needs when they receive insufficient energy or require structural material to build membranes. Hormones of the body that have a lipolytic effect - adrenaline, glucagon, somatotropin, cortisol, thyroid hormones - send a signal to adipocytes - lipolysis or the process of fat breakdown occurs.

Having received “instructions” from hormones, triglycerides are broken down into fatty acids and glycerol. Fatty acids are transported into the blood using carriers called lipoproteins. Lipoproteins in the blood interact with cell receptors, which break down lipoproteins and take fatty acids for further oxidation and use: building membranes or producing energy. Lipolysis can be activated under stress, excessive physical activity.

4 Why is lipid metabolism disrupted?

Dyslipidemia or lipid metabolism disorder is a condition in which, due to various reasons, there is a change in the content of lipids in the blood (increase or decrease), or the appearance of pathological lipoproteins. The condition is caused by pathological processes in the synthesis, breakdown of fats or their inadequate removal from the blood. Problems in lipid metabolism can lead to excess fat in the blood - hyperlipidemia.

According to research, this condition is typical for 40% of the adult population, and occurs even in childhood.

Disorders of lipid metabolism can be provoked by a number of factors that trigger pathological processes of imbalance in the supply and utilization of lipids. Risk factors include:

physical inactivity or a sedentary lifestyle,
smoking,
alcohol abuse,
increased activity of thyroid hormones,
excess body weight,
diseases that provoke lipid metabolic disorders.

5 Primary disorders of lipid metabolism

All lipid metabolism disorders are classified into primary and secondary. Primary ones are caused by genetic defects and are hereditary in nature. There are several forms of primary disorders in lipid metabolism, the most common being familial hypercholesterolemia. This condition is caused by a defect in the gene encoding the synthesis and function of receptors that bind to certain lipoproteins. There are several forms of pathology (homo- and heterozygous), they are united by the hereditary nature of the disease, high cholesterol levels from birth, early development atherosclerosis and ischemic heart disease.

A doctor may suspect hereditary dyslipoproteinemia in a patient if:

early myocardial infarction;
significant damage to blood vessels by the atherosclerotic process at a young age;
available data on the incidence of coronary artery disease and cardiovascular accidents in close relatives at a young age.

6 Secondary disorders of lipid metabolism

These lipid metabolism disorders develop as a consequence of many diseases, as well as as a result of the use of certain medications.

Causes of high blood lipids:

diabetes,
obesity,
hypothyroidism,
taking medications: progesterone, thiazides, estrogens, glucocorticoids,
chronic renal failure,
stress.

Reasons for low lipid levels:

malabsorption syndrome,
reduced, insufficient nutrition,
tuberculosis,
chronic liver diseases,
AIDS.

Dyslipidemia of secondary origin is very often observed in type 2 diabetes mellitus. It is always accompanied by atherosclerosis - changes in the walls of blood vessels with the deposition of “plaques” of excess cholesterol and other lipid fractions on them. Among patients with diabetes, the most common cause of death is coronary artery disease caused by atherosclerotic disorders.

7 Consequences of high blood lipids

Excessively “fatty” blood is enemy number 1 for the body. Excessive amounts of lipid fractions, as well as defects in their utilization, inevitably lead to the fact that “everything unnecessary” settles on vascular wall with the formation of atherosclerotic plaques. Exchange lipid disorders lead to the development of atherosclerosis, which means that in such patients the risk of developing coronary heart disease, stroke, and heart rate.

8 Signs indicating lipid metabolism disorders

An experienced physician may suspect dyslipidemia in a patient upon examination. External signs indicating existing advanced violations will be:

multiple yellowish formations - xanthomas, located on the torso, abdomen, forehead skin, as well as xanthelasmas - yellow spots on eyelids;
Men may experience early graying of hair on the head and chest;
matte ring around the edge of the iris.

All external signs are a relative indication of a lipid metabolism disorder, and to confirm it, a set of laboratory and instrumental studies is required to confirm the doctor’s assumptions.

9 Diagnosis of lipid metabolism disorders

There is an examination program to identify dyslipidemia, which includes:

general blood test, urine test,
BAC: determination of total cholesterol, TG, LDL cholesterol, VLDL, HDL, ASAT, ALAT, bilirubin, protein, protein fractions, urea, alkaline phosphatase,
determining blood glucose, and if there is a tendency to increase, performing a glucose tolerance test,
determination of abdominal circumference, Quetelet index,
blood pressure measurement,
Examination of the vessels of the fundus,
EchoCG,
radiography of the OGK.

This is a general list of studies, which in case of lipid metabolism disorders, at the discretion of the doctor, can be expanded and supplemented.

10 Treatment of lipid metabolism disorders

Therapy for secondary dyslipidemia is aimed, first of all, at eliminating the underlying disease that caused the disorder of lipid metabolism. Correction of glucose levels in diabetes mellitus, normalization of body weight in obesity, treatment of absorption disorders and in the gastrointestinal tract are guaranteed to improve lipid metabolism. Elimination of risk factors and a lipid-lowering diet for lipid metabolism disorders is the most important part on the path to recovery.

Patients should forget about smoking, stop drinking alcohol, lead an active lifestyle and combat physical inactivity. Food should be enriched with PUFAs (they contain liquid vegetable oils, fish, seafood), the overall consumption of fats and foods containing saturated fats should be reduced ( butter, eggs, cream, animal fat). Drug therapy for lipid metabolism disorders includes taking statins, fibrates, nicotinic acid, bile acid sequestrants according to indications.

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