Intermediate products of respiration processes serve as a source of carbon skeletons for the synthesis of lipids - fat-like substances that are part of all living cells and play an important role in life processes. Lipids act both as storage substances and as components of membranes surrounding the cytoplasm and all cellular organelles.

Membrane lipids differ from ordinary fats in that one of the three fatty acids in their molecule is replaced by phosphorylated serine or choline.

Fats are present in all plant cells, and since fats are insoluble in water, they cannot move around in plants. Therefore, the biosynthesis of fats must occur in all organs and tissues of plants from dissolved substances entering these organs. Such soluble substances are carbohydrates that enter the seeds from assimilating *. The best object for studying the biosynthesis of fats are the fruits of oilseeds; at the beginning of the development of oilseeds, the main components of the seeds are water, proteins, non-protein nitrogenous compounds and insoluble sugars. During ripening, on the one hand, the synthesis of proteins from non-protein nitrogenous compounds occurs, and on the other, the conversion of carbohydrates into fats.

We will focus on converting carbohydrates into fats. Let's start with something simple. From the composition of fats. Fats consist of glycerol and fatty acids. Obviously, during the biosynthesis of fats, these components must be formed - glycerol and fatty acids, which are part of the fat. During the biosynthesis of fat, it was discovered that fatty acids are combined not with bound glycerol, but with its phosphorylated * - glycerol-3phosphate. The starting material for the formation of glycerol-3phosphate is 3-phosphoglyceraldehyde and phosphodioxyacetone, which are intermediate products of photosynthesis and anaerobic breakdown of carbohydrates

The reduction of phosphodioxyacetone to glycerol-3phosphate is catalyzed by the enzyme glycerol phosphate dehydrogenase, the active group of which is nicotinamide adenine dinucleotide. The synthesis of fatty acids occurs in more complex ways. We have seen that most plant fatty acids have an even number of carbon atoms, C16 or C18. This fact has long attracted the attention of many researchers. It has been repeatedly suggested that fatty acids can be formed as a result of the free condensation of acetic acid or acetaldehyde, i.e. from compounds having two carbon atoms C 2. Works of our time have established that it is not free acetic acid that takes part in the biosynthesis of fatty acids, but acetyl coenzyme A bound to coenzyme A. Currently, it is fashionable to depict the scheme of fatty acid synthesis as follows. The starting compound for the synthesis of fatty acids is acetyl coenzyme A, which is the main product of the anaerobic breakdown of carbohydrates. Coenzyme A can take part in the synthesis of a wide variety of fatty acids. The first * of these processes is the activation of acids under the action of ATP. At the first stage, acetyl coenzyme A is formed from acetic acid under the action of the enzyme acetyl coenzyme A * and the expenditure of energy ATP and then * i.e. carboxylation of acetyl CoA occurs and the formation of a 3-carbon compound. At subsequent stages, condensation of the acetyl coenzyme A molecule occurs.

The synthesis of fatty acids occurs by binding the acetyl coenzyme A molecule. This is the first stage of the actual synthesis of fatty acids.

The general pathway for the formation of fats from carbohydrates can be represented as a diagram:

glycerol-3phosphate

Carbohydrates

Acetyl coenzyme A → fatty acid → fats

As we already know, fats can move from one plant tissue to another and they are synthesized directly in places of accumulation. The question arises: in what parts of the cell, in what cellular structures are they synthesized? In plant tissues, the biosynthesis of fats is almost completely localized in mitochondria and spherosomes. The rate of fat synthesis in cells is closely related to the intensity of oxidative processes, which are the main sources of energy. In other words, the biosynthesis of fats is closely related to respiration.

The breakdown of fats occurs most intensively during the germination of oilseed seeds. Oilseeds contain few carbohydrates and the main reserve substances in them are fats. Fats differ from carbohydrates and proteins not only in that their oxidation releases significantly more energy, but also in that the oxidation of fats releases an increased amount of water. If the oxidation of 1 g of proteins produces 0.41 g of water, the oxidation of 1 g of carbohydrates produces 0.55 g, then the oxidation of 1 g of fat produces 1.07 g of water. This is of great importance for the developing embryo, especially when seeds germinate in dry conditions.

In works related to the study of the breakdown of fats, it has been proven that in germinating seeds, along with the loss of fats, carbohydrates accumulate. In what ways can carbohydrates be synthesized from fats? In general form, this process can be represented as follows. Fats are broken down into glycerol and fatty acids by lipase with the participation of water. Glycerol is phosphorylated, then oxidized and converted to 3-phosphoglyceraldehyde. 3-phosphoglyceraldehyde isomerizes to give phosphodioxyacetone. Further, under the influence of * and 3-phosphoglyceraldehyde and phosphodioxyacetone, fructose-1.6diphosphate is synthesized. The formed fructose-1.6 diphosphate, as we already know, is converted into a wide variety of carbohydrates, which serve to build plant cells and tissues.

What is the path of transformation of fatty acids that are cleaved off during the action of lipase on fats? At the first stage, the fatty acid, as a result of a reaction with coenzyme A and ATP, is activated and acetyl coenzyme A is formed

R CH 2 CH 2 COOH + HS-CoA + ATP → RCH 2 CH 2 C- S – CoA

Activated fatty acid, acetyl coenzyme A, is more reactive than free fatty acid. In subsequent reactions, the entire carbon chain of the fatty acid is split into two-carbon fragments of acetyl coenzyme A. The general scheme of fat breakdown can be presented in a simplified form as follows.

Conclusion on the synthesis of fat breakdown. Both during the breakdown and synthesis of fatty acids, the main role belongs to acetyl coenzyme A. Acetyl coenzyme A formed as a result of the breakdown of fatty acids can further undergo various transformations. The main path of its transformation is complete oxidation through the tricarboxylic acid cycle to CO 2 and H 2 O with the release of a large amount of energy. Part of acetyl coenzyme A can be used for the synthesis of carbohydrates. Such transformations of acetyl coenzyme A can occur during the germination of oilseeds, when a significant amount of acetic acid is formed as a result of the amino acid breakdown of fatty acids. During the biosynthesis of carbohydrates from acetyl coenzyme A OH, i.e. acetyl coenzyme A is included in the so-called glyoxylate cycle or glyoxic acid cycle. In the glyoxylate cycle, isocitric acid is split into succinic and glyoxic acids. Succinic acid can take part in the reaction of the tricarboxylic acid cycle and, through *, form malic and then oxaloacetic acid. Glyoxynic acid enters into CO compounds with a second molecule of acetyl coenzyme A and, as a result, malic acid is also formed. In subsequent reactions, malic acid is converted into oxalic-acetic acid - phosphoenolpyruvic acid - phosphoglyceric acid and even carbohydrates. Thus, the energy of the acids of the acetate molecule formed during the breakdown is converted into carbohydrates. What is the biological role of the glyoxylate cycle? In the reactions of this cycle, glyoxylic acid is synthesized, which serves as the starting compound for the formation of the amino acid glycine. The main role is due to the existence of the glyoxylate cycle, acetate molecules formed during the breakdown of fatty acids are converted into carbohydrates. Thus, carbohydrates can be formed not only from glycerol, but also from fatty acids. The synthesis of the final photosynthetic assimilation products, carbohydrates, sucrose and starch in a photosynthetic cell is carried out separately: sucrose is synthesized in the cytoplasm, starch is formed in chloroplasts.

Conclusion. Sugars can be enzymatically converted from one to another, usually with the participation of ATP. Carbohydrates are converted into fats through a complex chain of biochemical reactions. Carbohydrates can be synthesized from fat breakdown products. Carbohydrates can be synthesized from both glycerol and fatty acids.

Lipid biosynthesis

Triacylglycerols are the most compact form of energy storage in the body. Their synthesis is carried out mainly from carbohydrates that enter the body in excess and are not used to replenish glycogen stores.

Lipids can also be formed from the carbon skeleton of amino acids. Promotes the formation of fatty acids, and subsequently triacylglycerols and excess food.

Biosynthesis of fatty acids

During oxidation, fatty acids are converted to acetyl-CoA. Excessive dietary intake of carbohydrates is also accompanied by the breakdown of glucose into pyruvate, which is then converted into acetyl-CoA. This latter reaction, catalyzed by pyruvate dehydrogenase, is irreversible. Acetyl-CoA is transported from the mitochondrial matrix to the cytosol as part of citrate (Figure 15).

Mitochondrial matrix Cytosol

Figure 15. Scheme of acetyl-CoA transfer and the formation of reduced NADPH during fatty acid synthesis.

Stereochemically, the entire process of fatty acid synthesis can be represented as follows:

Acetyl-CoA + 7 Malonyl-CoA + 14 NADPH∙ + 7H + 

Palmitic acid (C 16:0) + 7 CO 2 + 14 NADP + 8 NSCoA + 6 H 2 O,

in this case, 7 molecules of malonyl-CoA are formed from acetyl-CoA:

7 Acetyl-CoA + 7 CO 2 + 7 ATP  7 Malonyl-CoA + 7 ADP + 7 H 3 PO 4 + 7 H +

The formation of malonyl-CoA is a very important reaction in fatty acid synthesis. Malonyl-CoA is formed in the carboxylation reaction of acetyl-CoA with the participation of acetyl-CoA carboxylase, which contains biotin as a prosthetic group. This enzyme is not part of the fatty acid synthase multienzyme complex. Acetite carboxylase is a polymer (molecular weight from 4 to 810 6 Da), consisting of protomers with a molecular weight of 230 kDa. It is a multifunctional allosteric protein containing bound biotin, biotin carboxylase, transcarboxylase and an allosteric center, the active form of which is a polymer, and the 230-kDa protomers are inactive. Therefore, the activity of malonyl-CoA formation is determined by the ratio between these two forms:

Inactive protomers  active polymer

Palmitoyl-CoA, the final product of biosynthesis, shifts the ratio towards the inactive form, and citrate, being an allosteric activator, shifts this ratio towards the active polymer.

Figure 16. Mechanism of synthesis of malonyl-CoA

In the first step of the carboxylation reaction, bicarbonate is activated and N-carboxybiotin is formed. At the second stage, a nucleophilic attack of N-carboxybiotin by the carbonyl group of acetyl-CoA occurs and malonyl-CoA is formed in the transcarboxylation reaction (Fig. 16).

Fatty acid synthesis in mammals is associated with a multienzyme complex called fatty acid synthase. This complex is represented by two identical multifunctional polypeptides. Each polypeptide has three domains, which are located in a specific sequence (Fig.). First domain is responsible for binding acetyl-CoA and malonyl-CoA and connecting these two substances. This domain includes the enzymes acetyltransferase, malonyltransferase, and an acetyl-malonyl-binding enzyme called -ketoacyl synthase. Second domain, is primarily responsible for the reduction of the intermediate obtained in the first domain and contains acyl transfer protein (ACP), -ketoacyl reductase and dehydratase and enoyl-ACP reductase. IN third domain the enzyme thioesterase is present, which releases the resulting palmitic acid, consisting of 16 carbon atoms.

Rice. 17. Structure of the palmitate synthase complex. The numbers indicate domains.

Mechanism of fatty acid synthesis

At the first stage of fatty acid synthesis, acetyl-CoA is added to the serine residue of acetyltransferase (Fig...). In a similar reaction, an intermediate is formed between malonyl-CoA and the serine residue of malonyltransferase. The acetyl group from the acetyltransferase is then transferred to the SH group of the acyl transfer protein (ATP). At the next stage, the acetyl residue is transferred to the SH group of the cysteine ​​of -ketoacyl synthase (condensing enzyme). The free SH group of the acyl-transfer protein attacks the malonyltransferase and binds the malonyl residue. Then condensation of the malonyl and acetyl residues occurs with the participation of -ketoacyl synthase with the removal of the carbonyl group from the malonyl. The result of the reaction is the formation of -ketoacyl associated with ACP.

Rice. Reactions of 3-ketoacylACP synthesis in the palmitate synthase complex

The enzymes of the second domain then participate in the reduction and dehydration reactions of the β-ketoacyl-ACP intermediate, which result in the formation of (butyryl-ACP) acyl-ACP.

Acetoacetyl-ACP (-ketoacyl-ACP)

-ketoacyl-ACP reductase

-Hydroxybutyryl-APB

-hydroxyacyl-ACP dehydratase

Enoyl-ACP reductase

Butyryl-APB

After 7 reaction cycles

H2O palmitoylthioesterase

The butyryl group is then transferred from ACP to the cis-SH residue of -ketoacyl synthase. Further extension by two carbons occurs by addition of malonyl-CoA to the serine residue of malonyltransferase, then condensation and reduction reactions are repeated. The entire cycle is repeated 7 times and ends with the formation of palmitoyl-ACP. In the third domain, palmitoyl esterase hydrolyzes the thioester bond into palmitoyl-ACP and free palmitic acid is released and leaves the palmitate synthase complex.

Regulation of fatty acid biosynthesis

The control and regulation of fatty acid synthesis is, to a certain extent, similar to the regulation of the reactions of glycolysis, the citrate cycle, and β-oxidation of fatty acids. The main metabolite involved in the regulation of fatty acid biosynthesis is acetyl-CoA, which comes from the mitochondrial matrix as part of citrate. The malonyl-CoA molecule formed from acetyl-CoA inhibits carnitine acyltransferase I and β-oxidation of fatty acid becomes impossible. On the other hand, citrate is an allosteric activator of acetyl-CoA carboxylase, and palmitoyl-CoA, steatoryl-CoA and arachidonyl-CoA are the main inhibitors of this enzyme.

Contents: - biosynthesis of saturated FAs - biosynthesis of unsaturated FAs - biosynthesis. TG and phosphatides - cholesterol biosynthesis. Pool of cholesterol in the cell - mechanism for regulating carbohydrate metabolism - fat-carbohydrate Randle cycle

Biosynthesis of FA occurs most intensively in the gastrointestinal tract, hepatocytes, enterocytes, and lactating mammary gland. The source of carbon for FA biosynthesis is excess carbohydrates, amino acids, and FA metabolism products.

FA biosynthesis is an alternative version of ßoxidation, but carried out in the cytoplasm. The oxidation process produces energy in the form of FADH 2, NADH 2 and ATP, and FA biosynthesis absorbs it in the same form.

The starting substrate for the synthesis is acetyl-Co. A, formed in the mitochondrial matrix. The mitochondrial membrane is not permeable to acetyl-Co. And, therefore, it interacts with PKA to form citrate, which freely passes into the cytoplasm and there is broken down to PAA and acetyl. Co. A.

An increase in citrate in the cytoplasm is a signal for the beginning of FA biosynthesis. Citrate + ATP + NSCo. A ------ CH 3 -CO-SCo. A+ PIKE +ADP The reaction occurs under the action of citrate lyase.

For the synthesis of FA, one molecule of acetyl-Co is required. A, inactive, while the rest should be activated. CH 3 -CO-SCo. A + CO 2+ ATP + biotin-------------- COOH-CH 2 -CO-SCo. And Acetyl-Co. A-carboxylase The enzyme activator is Acetyl-Co. Acarboxylase is citrate. The first reaction in biosynthesis is the formation of malonyl-Co. A.

Malonil-Co. A is the initial intermediate in the synthesis of fatty acids, formed from acetyl-Co. And in the cytoplasm.

Excess acetyl-Co. And in mitochondria it cannot independently pass into the cytoplasm. Passage through the mitochondrial membrane is made possible by the citrate shunt. Acetyl-Co. And carboxylase catalyzes the formation of malonyl-Co. A.

This reaction consumes CO 2 and ATP. Thus, conditions that promote lipogenesis (presence of large amounts of glucose) inhibit β-oxidation of fatty acids

The biosynthesis of fatty acids is carried out using a multienzyme complex - palmitoyl fatty acid synthetase. It consists of 7 enzymes associated with ACP (acyl transport protein). APB consists of 2 subunits, each of which contains 250 thousand units. APB contains 2 SH groups. After the formation of malonyl-Co. And the transfer of acetyl and malonyl residues to APB occurs.

Biosynthesis of FAs will occur at high levels of glucose in the blood, which determines the intensity of glycolysis (supplier of acetyl-Co. A), PPP (supplier of NADFH 2 and CO 2). Under conditions of fasting and diabetes, GI synthesis is unlikely, because no. Gl (in diabetes, it does not enter the tissues, but is in the blood), therefore the activity of glycolysis and PPP will be low.

But under these conditions, there are reserves of CH 3 -COSCo in the liver mitochondria. A (source of ß-oxidation of FA). However, this acetyl-Co. And does not enter into reactions of FA synthesis, since it must be limited by the products PC, CO 2 and NADH 2. In this case, it is more profitable for the body to synthesize cholesterol, which requires only NADFH 2 and acetyl-Co. What happens during fasting and diabetes?

Biosynthesis of TG and PL Synthesis of TG occurs from Glycerol (Gn) and FA, mainly stearic and palmitic oleic. The biosynthesis of TG in tissues proceeds through the formation of glycerol-3 phosphate as an intermediate compound. In the kidneys and enterocytes, where glycerol kinase activity is high, Gn is phosphorylated by ATP to glycerol phosphate.

In adipose tissue and muscle, due to the very low activity of glycerol kinase, the formation of glycero-3-phosphate is mainly associated with glycolysis. It is known that glycolysis produces DAP (dihydroxyacetone phosphate), which, in the presence of glycerol phosphate-DG, can be converted into G-3 ph (glycerol-3 phosphate).

In the liver, both pathways of g-3-ph formation are observed. In cases where the Glucose content in FA is reduced (during fasting), only a small amount of G-3-ph is formed. Therefore, FAs released as a result of lipolysis cannot be used for resynthesis. Therefore, they leave the VT and the amount of reserve fat decreases.

Synthesis of unsaturated fatty acids from saturated fatty acids with parallel chain extension. Desaturation occurs under the action of a microsomal enzyme complex consisting of three protein components: cytochrome b 5, cytochrome b 5 reductase and desaturase, which contain non-heme iron.

NADPH and molecular oxygen are used as substrates. These components form a short electron transport chain, with the help of which hydroxyl groups are included in the fatty acid molecule for a short period of time

They are then split off as water, resulting in a double bond being formed in the fatty acid molecule. There is a whole family of desaturase subunits that are specific to a particular site of insertion of the double bond.

The origin of unsaturated fatty acids in the cells of the body. Metabolism of arachidonic acid n Essential and non-essential - Among unsaturated fatty acids, -3 and -6 fatty acids cannot be synthesized in the human body due to the lack of an enzyme system that could catalyze the formation of a double bond at the -6 position or any other position closely located by the end.

These fatty acids include linoleic acid (18: 2, 9, 12), linolenic acid (18: 3, 9, 12, 15) and arachidonic acid (20: 4, 5, 8, 11, 14). The latter is essential only in cases of linoleic acid deficiency, since normally it can be synthesized from linoleic acid

Dermatological changes have been described in humans with a lack of essential fatty acids in food. The typical adult diet contains sufficient amounts of essential fatty acids. However, newborns who receive a diet low in fat show signs of skin lesions. They go away if linoleic acid is included in the course of treatment.

Cases of such deficiency are also observed in patients who have been on parenteral nutrition depleted in essential fatty acids for a long time. To prevent this condition, it is enough that the body receives essential fatty acids in an amount of 1-2% of the total caloric requirement.

Synthesis of unsaturated fatty acids from saturated fatty acids with parallel chain extension. Desaturation occurs under the action of a microsomal enzyme complex consisting of three protein components: cytochrome b 5, cytochrome b 5 reductase and desaturase, which contain non-heme iron. NADPH and molecular oxygen are used as substrates.

From these components, a short electron transport chain is formed, with the help of which hydroxyl groups are included in the fatty acid molecule for a short period of time. They are then split off as water, resulting in a double bond being formed in the fatty acid molecule. There is a whole family of desaturase subunits that are specific to a particular site of insertion of the double bond.

Formation and utilization of ketone bodies n The two main types of acetone bodies are acetoacetate and hydroxybutyrate. -Hydroxybutyrate is the reduced form of acetoacetate. Acetoacetate is formed in liver cells from acetyl~Co. A. Formation occurs in the mitochondrial matrix.

The initial stage of this process is catalyzed by the enzyme ketothiolase. Then acetoacetyl. Co. A condenses with the next acetyl-Co molecule. And under the influence of the enzyme HOMG-Co. And synthetases. As a result, -hydroxy-methylglutaryl-Co is formed. A. Then the enzyme HOMG-Co. And lyase catalyzes the cleavage of HOMG-Co. And for acetoacetate and acetyl-Co. A.

Subsequently, acetoacetic acid is reduced under the influence of the enzyme b-hydroxybutyrate dehydrogenase, resulting in the formation of b-hydroxybutyric acid.

Then the enzyme is HOMG-Co. And lyase catalyzes the cleavage of HOMG-Co. And for acetoacetate and acetyl. Co. A. Subsequently, acetoacetic acid is reduced under the influence of the enzyme b-hydroxybutyrate dehydrogenase, resulting in the formation of b-hydroxybutyric acid.

n these reactions occur in mitochondria. The cytosol contains isoenzymes - ketothiolases and HOMG~Co. And synthetases that also catalyze the formation of HOMG~Co. A, but as an intermediate product in the synthesis of cholesterol. Cytosolic and mitochondrial funds of GOMG~Co. But they don't mix.

The formation of ketone bodies in the liver is controlled by nutritional status. This control effect is enhanced by insulin and glucagon. Eating and insulin reduce the formation of ketone bodies, while fasting stimulates ketogenesis due to an increase in the amount of fatty acids in cells

During fasting, lipolysis increases, glucagon levels and c concentration increase. AMP in the liver. Phosphorylation occurs, thereby activating HOMG-Co. And synthetases. Allosteric inhibitor of HOMG-Co. And the synthetase is succinyl-Co. A.

n Normally, ketone bodies are a source of energy for muscles; during prolonged fasting, they can be used by the central nervous system. It should be borne in mind that the oxidation of ketone bodies cannot take place in the liver. In the cells of other organs and tissues it occurs in mitochondria.

This selectivity is due to the localization of the enzymes that catalyze this process. First, α-hydroxybutyrate dehydrogenase catalyzes the oxidation of hydroxybutyrate to acetoacetate in an NAD+-dependent reaction. Then using the enzyme, succinyl Co. A Acetoacetyl Co. A transferase, coenzyme A moves with succinyl Co. And for acetoacetate.

Acetoacetyl Co is formed. A, which is an intermediate product of the last round of fatty acid oxidation. This enzyme is not produced in the liver. That is why oxidation of ketone bodies cannot occur there.

But a few days after the start of fasting, expression of the gene encoding this enzyme begins in brain cells. The brain thereby adapts to using ketone bodies as an alternative energy source, reducing its need for glucose and protein.

Thiolase completes the cleavage of acetoacetyl-Co. And, embedding Co. And at the place where the bond between and carbon atoms is broken. As a result, two acetyl-Co molecules are formed. A.

The intensity of oxidation of ketone bodies in extrahepatic tissues is proportional to their concentration in the blood. The total concentration of ketone bodies in the blood is usually below 3 mg/100 ml, and the average daily urinary excretion is approximately 1 to 20 mg.

Under certain metabolic conditions, when intense oxidation of fatty acids occurs, significant amounts of so-called ketone bodies are formed in the liver.

The condition of the body in which the concentration of ketone bodies in the blood is higher than normal is called ketonemia. An increased level of ketone bodies in the urine is called ketonuria. In cases where severe ketonemia and ketonuria occur, the smell of acetone is felt in the exhaled air.

It is caused by the spontaneous decarboxylation of acetoacetate to acetone. These three symptoms of ketonemia, ketonuria and the smell of acetone on breath are combined under the common name - ketosis

Ketosis occurs as a result of a lack of available carbohydrates. For example, during fasting, little of them is supplied (or not supplied) with food, and in diabetes mellitus, due to a lack of the hormone insulin, when glucose cannot be effectively oxidized in the cells of organs and tissues.

This leads to an imbalance between esterification and lipolysis in adipose tissue towards the intensification of the latter. It is caused by the spontaneous decarboxylation of acetoacetate to acetone.

The amount of acetoacetate that is reduced to -hydroxybutyrate depends on the NADH/NAD+ ratio. This restoration occurs under the influence of the enzyme hydroxybutyrate dehydrogenase. The liver serves as the main site for the formation of ketone bodies due to the high content of HOMG-Co. And synthetases in the mitochondria of hepatocytes.

Biosynthesis of cholesterol CS is synthesized by hepatocytes (80%), enterocytes (10%), kidney cells (5%), and skin. 0.3-1 g of cholesterol is formed per day (endogenous pool).

Functions of cholesterol: - An indispensable participant in cell membranes - Precursor of steroid hormones - Precursor of bile acids and vitamin D

After the breakdown of polymer lipid molecules, the resulting monomers are absorbed in the upper part of the small intestine in the initial 100 cm. Normally, 98% of dietary lipids are absorbed.

1. Short fatty acids(no more than 10 carbon atoms) are absorbed and pass into the blood without any special mechanisms. This process is important for infants because... milk contains mainly short- and medium-chain fatty acids. Glycerol is also absorbed directly.

2. Other digestion products (long-chain fatty acids, cholesterol, monoacylglycerols) form with bile acids micelles with a hydrophilic surface and a hydrophobic core. Their sizes are 100 times smaller than the smallest emulsified fat droplets. Through the aqueous phase, the micelles migrate to the brush border of the mucosa. Here the micelles break down and the lipid components diffuse inside the cell, after which they are transported to the endoplasmic reticulum.

Bile acids also here they can enter enterocytes and then go into the blood of the portal vein, but most of them remain in the chyme and reach ileal intestines, where it is absorbed through active transport.

Resynthesis of lipids in enterocytes

Lipid resynthesis is the synthesis of lipids in the intestinal wall from exogenous fats entering here; both can be used at the same time endogenous fatty acids, therefore resynthesized fats differ from food fats and are closer in composition to “their” fats. The main task of this process is to tie medium- and long-chain ingested from food fatty acid with alcohol - glycerol or cholesterol. This, firstly, eliminates their detergent effect on membranes and, secondly, creates their transport forms for transport through the blood to tissues.

The fatty acid entering the enterocyte (as well as any other cell) is necessarily activated through the addition of coenzyme A. The resulting acyl-SCoA participates in the reactions of the synthesis of cholesterol esters, triacylglycerols and phospholipids.

Fatty acid activation reaction

Resynthesis of cholesterol esters

Cholesterol is esterified using acyl-SCoA and the enzyme acyl-SCoA:cholesterol acyltransferase(AHAT).

Reesterification of cholesterol directly affects its absorption into the blood. Currently, possibilities are being sought to suppress this reaction to reduce the concentration of cholesterol in the blood.

Cholesterol ester resynthesis reaction

Resynthesis of triacylglycerols

There are two ways to resynthesize TAG:

The first way, the main one - 2-monoacylglyceride– occurs with the participation of exogenous 2-MAG and FA in the smooth endoplasmic reticulum of enterocytes: the multienzyme complex of triacylglycerol synthase forms TAG.

Monoacylglyceride pathway for TAG formation

Since 1/4 of the TAG in the intestine is completely hydrolyzed, and glycerol is not retained in the enterocytes and quickly passes into the blood, a relative excess of fatty acids arises for which there is not enough glycerol. Therefore there is a second one, glycerol phosphate, a pathway in the rough endoplasmic reticulum. The source of glycerol-3-phosphate is the oxidation of glucose. The following reactions can be distinguished:

1. Formation of glycerol-3-phosphate from glucose.
2. Conversion of glycerol-3-phosphate to phosphatidic acid.
3. Conversion of phosphatidic acid to 1,2-DAG.
4. Synthesis of TAG.

Glycerol phosphate pathway for TAG formation

Resynthesis of phospholipids

Phospholipids are synthesized in the same way as in other cells of the body (see "Phospholipid synthesis"). There are two ways to do this:

The first route is using 1,2-DAG and the active forms of choline and ethanolamine to synthesize phosphatidylcholine or phosphatidylethanolamine.