Question No. 40. Digestion of tag of pancreatic lipase. Digestion of phospholipids, intersectated cholesterol. Suction of hydrolysis products into the intestine mucous membrane. Mixel education.
Fat digestion occurs in the small intestine. The action of pancreatic lipase, hydrolyzing fats, precedes fats emulsification. Emulsification (mixing fat with water) occurs in the small intestine under the action of hydrochloric acid salts. Emulsification leads to an increase in the surface area of \u200b\u200bthe phase of fat / water, which accelerates the hydrolysis of fat with pancreatic lipase.
Fat digestion - hydrolysis of fats with pancreatic lipase. The optimal pH value for the pancreatic lipase is achieved by neutralizing the acid content coming from the stomach, bicarbonate highlighted in the pancreatic juice
Pancreatic lipase is distinguished into the cavity of the small intestine from the pancreas along with the protein colipase. Colipase contributes to the formation of such a conformation of pancreatic lipase, in which the active center of the enzyme is as close as possible to its substrates - fat molecules.
Pancreatic lipase hydrolyzes fats primarily in positions 1 and 3, so the main products of hydrolysis are free fatty acids and 2-monocylglycerol (β-monoacilglycerol).
In the digestion of glycelofospholipids, several enzymes are involved, synthesized in the pancreas.
Hydrolysis of cholesterol ethers occurs under the action of cholesterol easerase - enzyme, which is also synthesized in the pancreas and secreted into the intestine. Hydrolysis products (cholesterol and fatty acids) are absorbed in the composition of mixed micelles.
Lipid hydrolysis products - fatty acids with a long hydrocarbon radical, 2-monoacylglycerol, cholesterol, as well as salts of greyhounds form in the lumen of the intestine of the structure, called mixed micelles. Mixed micelles are constructed in such a way that the hydrophobic parts of the molecules are addicted inside the micelles, and hydrophilic - outward, so micelles are well dissolved in the aqueous phase of the contents of the small intestine. Micelles are brought together with the brush border of the cishetic mucosa cells, and the lipid components of micelles diffuse through the membranes inside the cells.
Suction of fatty acids with an average chain length formed, for example, when digesting milk lipids, occurs without the participation of mixed micelles. These fatty acids from the cell mucosa cells of the small intestine fall into the blood, bind to the protein albumin and are transported to the liver.
Question No. 41. Bile acids, their structure, biosynthesis. Conjugation of bile acids. Their role in digestion and suction of lipids. Steatery.
Handic acids - cholesterol derivatives with a five-carbon side chain in position 17, which ends with a carboxyl group. In the human body, two galls are synthesized: a chill, which contains three hydroxyl groups in positions 3, 7, 12, and hanodoxychole, containing two hydroxyl groups in positions 3 and 7. They are not effective emulsifiers.
Handic acids are synthesized in cholesterol liver.
In the liver, the emulsifying properties of gall acids increase due to the reaction of the conjugation, in which taurine or glycine is joined to the carboxyl group. These derivatives are conjugated handicacious acids - are in ionized form and therefore are called hydraulic acid salts. It is they who serve as the main emulsifiers of fats in the intestine.
As fats - Insoluble in water compounds, they may be subjected to enzymes dissolved in water only on the border of the phase separation water / fat. Therefore, the action of pancreatic lipase, hydrolyzing fats, is preceded by fats emulsification. Emulsification (mixing fat with water) occurs in the small intestine under the action of hydrochloric acid salts. Emulsification leads to an increase in the surface area of \u200b\u200bthe phase of fat / water, which accelerates the hydrolysis of fat with pancreatic lipase. In addition, the salts of bile acids ensure the stability of the micelles, thus contributing to the suction of liquid hydrolysis products into the blood.
Disruption of digestion Fats may be a consequence of several reasons. One of them is a violation of the secretion of yellow bubble with a mechanical obstacle to the outflow of yellow. Reducing the secretion of yellow leads to a violation of the emulsification of food fats and, consequently, to a decrease in the ability of pancreatic lipase to hydrolyze fats.
Violation of the secretion of the pancreas juice and, therefore, the insufficient secretion of pancreatic lipase also lead to a decrease in the hydrolysis rate of fats. In both cases, the disruption of digestion and suction of fat leads to an increase in the number of fats in feces - there is a steatheree (bold chair). Normally, the fat content in feces is no more than 5%. With steamer, absorption of fat-soluble vitamins (A, D, E, K) and essential fatty acids are disturbed.
Similar information.
Handic acids (LCD) are formed exclusively in the liver. Daily 250-500 mg of LCD is synthesized and lost with the feces. Synthesis LCD is regulated by a negative feedback mechanism. The primary LCD is synthesized from Xc: chill and hanodoxychole. The synthesis is regulated by the amount of LCD, which are returned to the liver in the process of enterohepatic circulation. Under the action of the bowel bacteria, the primary LCD is subjected to 7a-dehydroxylation with the formation of secondary LCD: deoxychole and very slight amount of lithochole. Tertiary LCD, mainly ursodeoxychole, are formed in the liver by isomerization of secondary LCD. In the Holy Human, the amount of trihydroxy acid (chic acid) is approximately equal to the sum of the concentrations of two-dimenshotslot - hanodoxychole and deoxychole.
LCD are connected in liver with amino acids glycine or taurine. This prevents their suction in the grying paths and the small intestine, but does not prevent suction in the terminal department of the ileum. Sulfatization and glucooner (which are detoxification mechanisms) can be intensified during cirrhosis or cholestasis, in which the excess of these conjugates are detected in the urine and yellow. Bacteria can hydrolyze salts of LCD on LCD and glycine or taurine.
Salts of the LCD are excreted into the horizontal tubules against a large concentration gradient between hepatocytes and yellow. Excretion is partially depends on the value of intracellular negative potential, which is approximately 35 mV and provides potential-dependent accelerated diffusion, as well as from the mediated by the carrier (glycoprotein with a molecular weight of 100 kDa) of the diffusion process. Salts of the LCD penetrate the micelles and bubbles, connecting with hs and phospholipids. In the upper sections of the small intestine of micelles of the salts of the LCD, quite large in size, have hydrophilic properties, which prevents their absorption. They are involved in digestion and suction of lipids. In the terminal department of the ileum and the proximal part of the colon, absorption of the LCD takes place, and in the ileum, suction takes place by active vehicle. Passive diffusion of non-ionized LCD occurs on all over the intestine and is the most effective in relation to non-conjugated dihydroxy-LC. Oral admission of ursodeoxycholic acid disrupts the suction of hanodoxychole and chokes in the small intestine.
The absorbed salts of the LCD fall into the system of the portal vein and in the liver, where they are intensively captured by hepatocytes. This process occurs due to the functioning of a friendly transport system of molecules through a sinusoidal membrane based on a Na + gradient. In this process, ions C1 are also involved. The most hydrophobic LCDs (unrelated mono- and dihydroxy gully acids) are likely to penetrate the hepatocyte by simply diffusion (according to the "Flip-flop" mechanism) through a lipid membrane. It remains unclear the mechanism of transport Z K through hepatocytes from sinusoids to the handwrites. In this process, binding LCD cytoplasmic proteins, such as hydroxysteroiddehydehydrogenase, are involved. The role of microtubule is unknown. Vesiculs are involved in the transfer of the LC only at a high concentration of the latter. The LCD is repeatedly conjugated and re-released in the horizontal. Lithocholic acid is not re-excursted.
The described Enterogeptic circulation of the LCD takes place from 2 to 15 times a day. The absorption capacity of various LCDs, as well as the speed of their synthesis and exchange, non-etinakov.
When cholestuz, the LCD is excreted with the urine by active transport and passive diffusion. LCD sulphables, the resulting conjugates are actively secreted by renal tubules.
Handic acids with liver diseases
LCD enhance excretion with water, lecithin, hs and the associated bilirubin fraction. Ursodeoxycholic acid leads to significantly greater herbal flow than hanodoxychole or chill.
An important role in the formation of the stones of the gorgeous bubble is played by violation of the excretion of the yellow and defect formation of greyhole micelles). It also leads to a steamer when cholestuz.
LCD, connecting with hs and phospholipids, form a suspension of micelles in solution and, thus, contribute to the emulsification of food fats, participating in parallel during the suction process through the mucous membranes. Reducing the secretion of the LCD causes steatore. LCD promote lipolysis of pancreatic enzymes and stimulate the formation of gastrointestinal hormone hormones.
Violation of intrahepatic metabolism LCD can play an important role in the pathogenesis of cholestasis. It was previously believed that they contribute to the development of itching with cholestasis, but recent studies suggest that itching is due to other substances.
The hopping of the LCD into the blood in patients with jaundice leads to the formation of target cells in peripheral blood and removal of conjugated bilirubin with urine. If the LCD is deconged by the bacteria of the small intestine, then the free LCDs are absorbed at the same time. The formation of micelles and suction of fats are violated. This is partly explained by Malabsorption syndrome, complicating the course of diseases, which are accompanied by the stasal of intestinal content and the enhanced increasing bacteria in the small intestine.
The removal of the terminal department of the ileum is interrupted by enterohepaticheatic hepatic circulation and contributes to the fact that a large number of primary LCD reaches the colon and dehydroxylized by bacteria, thereby reducing the Poland of the LC in the body. An increase in the amount of LCD in the colon causes diarrhea with a significant loss of water and electrolytes.
Litocholic acid is excreted primarily with the feces, and only its insignificant part is absorbed. Its administration causes cirrhosis of the liver in experimental animals and is used to simulate a gallway disease. Taurolyitocholic acid also causes intrahepatic cholestasis, probably due to a violation of the current of the boat, independent of the LCD.
Handic acid serum
With the help of gas-liquid chromatography, you can fractionate the LCD, but this method is expensive and takes a lot of time.
The enzyme method is based on the use of 3-hydroxycenoiddehydehydrogenase of bacterial origin. The use of bioluminescent analysis capable of detecting the pectolar amounts of the LCD, made an enzyme method equal to immunoradiological. In the presence of the necessary equipment, the method is simple and inexpensive. The concentration of individual factions of the LCD can also be determined by the immunoradiological method; For this there are special sets.
The overall level of the LCD in serum reflects reabsorption from the intestine of those LCDs that were not extracted with the first passage through the liver. This value serves as a criterion for assessing the interaction between two processes: suction in the intestines and seizure in the liver. The level of the LCD in serum is more dependent on absorption in the intestine than from their extraction of the liver.
The increase in the level of the LCD in serum indicates a hepatobiliary disease. The diagnostic value of the level of the LCD in viral hepatitis and chronic liver diseases was lower than previously assumed. Nevertheless, this indicator is more valuable than the concentration of albumin in serum and prothrombin time, since it not only confirms the lesion of the liver, but also allows you to estimate its excretory function and the presence of porto-systemic blood shunting. The level of the LCD in serum is also prognostic value. With hivber syndrome, the concentration of LCD within the norm)
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