Bile acid in the intestines

Anion exchange resins are basic polymers with a high affinity for anions. Because different anions compete for binding to them, they can be used to sequester anions. Clinically used anion exchange resins such as cholestyramine are used to sequester bile acids in the intestine, thereby preventing their reabsorption. As a consequence, the absorption of exogenous cholesterol is decreased. The accompanying increase in low density lipoprotein (LDL)-receptors leads to the removal of LDL from the blood and, thereby, to a reduction of LDL cholesterol. This effect underlies the use of cholestyramine in the treatment of hyperlipidaemia. 

Hyperlipidemia. Bile acid binding resins such as cholestyramine sequester bile acids in the intestine,... 

A portion of the primary bile acids in the intestine is subjected to further changes by the activity of the intestinal bacteria. These include deconjugation and 7a-dehydroxylation, which produce the secondary bile acids, deoxycholic acid and hthocholic acid. 

Similarly, dietary fibers are known to interact with bile acids in the intestinal limien and thus increase bile salt excretion in feces, resulting in decreased munbers... 

The primary action of BARs is to bind bile acids in the intestinal lumen, with a concurrent interruption of enterohepatic circulation of bile acids, which decreases the bile acid pool size and stimulates hepatic synthesis of bile acids from cholesterol. Depletion of the hepatic pool of cholesterol results in an increase in cholesterol biosynthesis and an increase in the... 

Alternative potential strategies for reduction of mucosal secondary bile acid exposure are to target deconjugation of glycine/taurine bile salts by bacterial bile salt hydrolases and/or bacterial 7-dehydroxylation of primary bile acids to secondary bile acids. Sequestration of bile acids in the intestinal lumen using probiotic bacteria has also been proposed as an area for future research. ... 

Pharmacology Bile acid sequestering resins bind bile acids in the intestine to form an insoluble complex, which is excreted in the feces. This results in a partial removal of bile acids from the enterohepatic circulation, preventing their absorption. 

Mechanism of Action An antihyperlipoproteinemic that binds with bile acids in the intestine, forming an insoluble complex. Binding results in partial removal of bile acid from enterohepatic circulation. Therapeutic Effect Removes LDL cholesterol from plasma. 

Mechanism of Action A lipid-bile acid sequestrant and nonsystemic polymer that binds with bile acids in the intestines, preventing their reabsorption and removing them from the body Therapeutic Effect Decreases LDL cholesterol. Pharmacokinetics Not absorbed. Primarily eliminated in feces. 

In addition to treatment with the statins, hypercholesterolemia is sometimes treated with the use of nonabsorbable anion-exchange resins like cholestyramine (5.13) and colestipol, which sequester bile acid in the intestine, excrete them, and thus increase their synthesis in the liver by a feedback mechanism. Increased bile acid synthesis increases cholesterol metabolism and also decreases LDL concentrations. Unfortunately, these resins interfere with the absorption of other fats and fat-soluble vitamins (A, D, E, and K). They... 

The bile acid-binding agents are large polymeric cationic exchange resins that are insoluble in water. They bind bile acids in the intestinal lumen and prevent their reabsorption. The resin itself is not absorbed. 

The prototype of a bile acid-binding resin is cholestyramine. Cholestyramine is the chloride salt of a basic anion-exchange resin. Its mechanism of action involves exchanging its chloride ion for bile acids in the intestinal lumen. By binding these bile acids, cholestyramine prevents them from being reabsorbed and, hence, they are... 

Bile acid sequestrates are anion-exchange resins, which sequester bile acid in the intestine. Cholestyramine and colestipol are the most commonly used in this category, which by this mechanism prevents bile acid re-absorption and causes decreased absorption of exogenous cholesterol and increased metabolism of endogenous cholesterol into bile acid in the liver by preventing enterohepatic recirculation. This leads to an increased expression of LDL receptors in liver and causes increased removal of LDL from blood and reduces the LDL cholesterol in the plasma. 

Binds bile acids in the intestine, thus preventing their return to the liver via the enterohepatic circulation. 

Colestyramine is an oral anion-exchange resin, which binds bile acids in the intestine. Bile acids are formed from cholesterol in the liver, pass into the gut in the bile and are largely reabsorbed at the terminal ileum. The total bile acid pool is only 3-5 g but, because such enterohepatic recycling takes place 5-10 times a day, on average 20-30 g of bile acid are delivered into the intestine every 24 hours. Bile acids bound to colestyramine are lost in the faeces and the depletion of the bile acid pool stimulates conversion of cholesterol to bile acid the result is a... 

Disposition of Bile Acids in the Intestines and Their Enterohepatic Circulation... 

Structures of bile acid sequestrants. Cholestyramine and colestipol are hydrophilic yet water-insoluble, nondigestible, and nonabsorbable synthetic resins. They bind bile acids in the intestine to increase their loss in feces and thereby decrease plasma cholesterol levels. 

Cholesterol-Reducing Agents. Hypercholesterolemia is well known as a major risk factor for coronary heart disease. In clinical practice, two main hypocholestrolemic agents are commonly used. One is the 3-hy-droxy-3-methylgrutaryl coenzyme A (HMG-CoA) reductase inhibitors (such as Lipitor) another is the bile acid sequestrants, such as cholestyramine and colestipol (97), which bind bile acid in the intestinal lumen and thus increase their excretion. The main drawback of... 

The mechanism of the inhibition of the HMG-CoA reductase by bile adds shown in Fig. 14 is a matter of controversy. Weis and Dietschy did not observe any influence of taurocholate on cholesterol synthesis in bile fistula rats fed a cholesterol-free diet, and concluded that the inhibitory effect of bile acids on cholesterol synthesis may be related to the increased absorption of cholesterol by the presence of bile acids in the intestine [247]. However, Hamprecht et al. were able to demonstrate a reduction of HMG-CoA reductase activity in lymph fistula rats infused with cholate [248]. Results by Shefer et al. also indicate that bile acids inhibit HMG-CoA reductase directly [212]. It seems likely that the inhibitory effect of the bile acids on HMG-CoA reductase may involve both direct and indirect effects. It was recently established that the stimulation of HMG-CoA reductase activity in response to treatment with cholestyramine is associated with an increase of the specific mRNA [258]. 

These bind bile acids in the intestine, increasing their excretion by preventing entero-hepatic recycling. This in turn causes the liver to use endogenous cholesterol for bile acid synthesis and circulating LDL levels fall. In addition, since bile acids are needed for cholesterol absorption this is reduced as well. Examples of bile acid sequestrants are colestipol and cholestyramine. 

Statins Ezitimibe Omega-3 triglycerides Bile acid sequestrants Fibrates Nicotinic acid derivatives Inhibit HMG-CoA reductase Inhibits absorption of cholesterol from the intestine Inhibit VLDL synthesis in the liver Bind bile acids in the intestine Lower levels of circulating VLDLs and LDLs by unknown mechanism Reduce the release of VLDLs from the liver... 

Cholestyramine is indicated as adjunctive therapy to diet for the reduction of elevated serum cholesterol in patients with primary hypercholesterolemia (elevated low-density lipoprotein [LDL] cholesterol) who do not respond adequately to diet. Similarly, it is indicated for the relief of pruritus associated with partial biliary obstruction. Cholestyramine is not absorbed but binds to bile acids in the intestine, whereupon it is eliminated. To replenish the lost bile acid, cholesterol is then converted to bile acid, and this lowers the level of cholesterol (see Figure 34). Cholestyramine has also been used in the treatment of cholestasis to control the intense pruritis. It reduces the LDL level in 4 to 7 days, and the maximum effect is seen in 14 days. 

Normally, most of the bile acids that are secreted into the intestine undergo reabsorption and are returned to the liver. Cholestyramine is a positively charged resin that binds bile acids in the intestinal lumen and prevents their reabsorption. 

The mechanism of this interaction would appear to be that the bile-acid binding resins bind with ursodeoxycholic acid (a bile acid) in the intestine and thereby reduce its absorption. 

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