The role of the liver in lipid metabolism.

Liver enzyme systems involved in the vast majority of reactions of lipid metabolism. These reactions provide for processes such as synthesis of fatty acids, triglycerides, phospholipids, cholesterol (relating to the lipids) and its esters, as well as lipolysis of triglycerides, fatty acid oxidation, the formation of acetone (ketone) phone, the synthesis of plasma lipoproteins.

It is known that the enzymatic reaction of triglyceride synthesis in liver and fat tissue are similar to marketing. Shin synthesized in the liver triglycerides or remain in the liver or secreted into the blood in the composition of lipoproteins, mainly VLDL (VLDL) and transported to the adipose tissue.

Part cholesterol (lipids related to sterol or sterols, ie, steroid alcohols) comes into contact with food, but much more of it is synthesized in the liver from acetate. The biosynthesis of cholesterol in the liver is inhibited exogenous cholesterol. Thus, the biosynthesis of cholesterol in the liver is governed by the principle negative feedback. The more cholesterol comes from food, the less than it is synthesized in the liver, and vice versa.

Part of the cholesterol synthesized in the liver out of the body together the bile, the other part is involved in the formation of bile acids, and is also used in other ­ gih bodies for Synthesis steroid hormones and other compounds.

Determination of cholesterol in the blood can be judged to some extent on the function the liver. In parenchyma ­ himatoznyh lesions of the liver synthetic activity of the cells is weakened, and the concentration of cholesterol in the blood decreases ­ Xia. Especially in these cases, reduced the concentration of cholesterol esters. In obstructive jaundice function hepatic disrupted cells is small (in uncomplicated cases), while at the same time ­ me a selection of cholesterol in the bile decreased sharply, which leads ­ leads to the increase in total cholesterol in the blood.

Diseases of the liver accompanied by a number of laboratory syndromes. In analyzing the results of biochemical studies in patients with liver disease it is advisable to allocate four laboratory syndrome, each of which corresponds to a certain extent a certain morphological and functional changes in the body: cytolytic syndrome, mesenchymal-inflammatory syndrome, cholestatic syndrome, small hepatocellular failure, usually in each case of the disease there is a combination of several biochemical syndromes.

Syndrome of the integrity of hepatocytes Syndrome (or cytolysis cytolytic syndrome).

Characterized by an increase in plasma tracer activity of enzymes - AST, ALT, LDH and its isoenzymes - LDG4 and LDG3; specific liver enzymes: fructose-1-fosfataldolazy, sorbitdegidrogenazy, as well as serum ferritin, serum iron, vitamin B12, and bilirubin is mainly due to increasing fraction of the line.

In assessing the severity of the pathological process of fundamental importance is attached to the activity of ALT and AST. Increase their level in the serum in less than five times compared with the upper limit of normal is seen as a moderate, 5 to 10 times - the average degree and more than 10 times - as high severity.
Morphological basis of this syndrome are acidophilic and hydropic degeneration and necrosis of hepatocytes with damage and increased permeability of cell membranes.

Cholestasis syndrome (excretory-biliary syndrome, cholestatic syndrome - a violation of the excretory function of the liver). Accompanied by increased levels of serum alkaline phosphatase, LAP, GGTF, cholesterol, P-lipoprotein fraction of conjugated bilirubin, bile acids, phospholipids, decreased excretion of bromsulfaleina (vofaverdina) radiofarmakologicheskih and drugs. Morphological basis of intracellular cholestasis are ultrastructural changes in hepatocytes - hyperplasia of smooth cytoplasmic network, changes in the biliary pole of hepatocytes, accumulation of bile components in the hepatocyte, which are often combined with cytolysis of hepatocytes. In intrahepatic cholestasis detect the accumulation of bile in the bile ducts, and in extrahepatic - expansion of interlobular bile ducts.

Syndrome of hepatocellular insufficiency syndrome (synthetic failure).

Manifested a decrease of serum total protein and especially albumin, transferrin, cholesterol, II, V, VII clotting factors, cholinesterase, alpha-lipoproteins, but at the same time, increased bilirubin due to unconjugated fraction. Morphological substrate of the syndrome are expressed dystrophic changes of hepatocytes and / or a significant decrease in functioning liver parenchyma as a result of necrotic changes.

Impaired function of hepatocytes can lead to a breach of albumin synthesis, which is observed in chronic liver diseases. The most pronounced hypoalbuminemia detected with portal cirrhosis, fatty liver.

Mesenchymal-inflammatory syndromes.

It is characterized by hypergammaglobulinemia, increased rates of protein-sediment samples, increased erythrocyte sedimentation rate, appearance of blood degradation products of connective tissue (C-reactive protein, seromucoid, etc.). For morphological studies of the liver characterized by activation and proliferation of lymphoid cells and retikulogistiotsitarnyh, increased fibrogenesis, the formation of the active septa with the necrosis of hepatocytes, intrahepatic migration of white blood cells, vasculitis.

If any damage to the liver may develop jaundice, which is often the first symptom of liver disease.

Jaundice is a yellow skin color is unnatural, or sclera. This is due to the presence of bilirubin in plasma at concentrations greater than 40 mmol / l. The normal concentration of bilirubin in the plasma of less than 22 mmol / l.

Bile pigments - breakdown products of hemoglobin and other derivatives of porphyrin excreted in the bile, urine, feces. The majority of them formed during the catabolism of hemoglobin in red blood cells in the decay of the cells of mononuclear phagocytes. Bile pigments are compounds containing four pyrrole groups linked one-carbon bridges in the open, non-closed circuit (in contrast to the closed structure of the heme). As a result, the gap a-methine bridge of heme in hemoglobin is formed verdoglobin (holeglobin) - iron-porphyrin pyrrole compound with an open structure, painted green. After cleavage of the protein molecule verdoglobina globin and iron produced green bile pigment biliverdin.An alternative way is formation of biliverdin cleavage of the protein part of hemoglobin, the pigment hematin formation zhelezoporfirinovogo and oxidation of hematin with a gap methine bridge and the loss of iron. In the cells of the mononuclear phagocyte system biliverdin is reduced to bilirubin

Every day produces about 300 mg of bilirubin.

Bilirubin slaborastvorim in water, primarily in the plasma bilirubin appears in the unconjugated form is associated with albumin (indirect, unconjugated bilirubin). Unconjugated bilirubin can not pass through the kidney barrier. In the liver there is a transition of bilirubin from albumin to the sinusoidal surface of hepatocytes. In liver cells exposed to enzymatic indirect bilirubin conjugation with glucuronic acid and is converted into bilirubinmono and bilirubindiglyukoronid (conjugated, direct, bilirubin).

Further metabolism of bilirubin is associated with the arrival of it in the biliary tract and intestines. In the lower parts of the biliary and intestinal microbial flora under the influence of a gradual recovery of conjugated bilirubin to urobilinogen. Part of urobilinogen (mezobilinogen) absorbed in the intestine and the portal vein re-enters the liver, where the norm is almost complete its destruction. Another part of urobilinogen (sterkobilinogen) is absorbed into the blood in the hemorrhoidal veins, getting into the bloodstream and excreted by the kidneys in the urine in small quantities in the form of urobilin, which is often not detected by clinical laboratory methods. Finally, the third part turns to sterkobilina urobilinogen and excreted in the feces, causing its characteristic dark brown color.

There are three main reasons for raising the level of bilirubin in the blood:

· The rate of synthesis of bilirubin is increased and exceeds the excretory capacity of the liver (hemolytic, nadpechenochnaya jaundice).

· Inhibition of conjugation and / or excretory mechanisms in the liver - reduces the liver's ability to metabolize synthesized in normal amounts of bilirubin (liver, hepatocellular jaundice).

· Obstruction of the biliary system, which prevents the outflow of bile flow (cholestatic, obstructive, mechanical, obstructive jaundice).

Date: 2014-12-21; view: 1359