Cholic acid is a primary bile acid that plays a role in fat digestion. It stabilizes lipids into emulsions, making them vulnerable to lipases. In the case of a cholic acid deficiency, fat digestion is disturbed, which is most noticeable in a change in stool consistency.
What is cholic acid?
Cholic acid is one of the two primary bile acids and is also known as 12α-trihydroxycholanic acid. The second bile acid in the primary form is called chenodesoxycholic acid. The starting material for the body’s production of the acids is cholesterol. The intermediate stage of production is pregnenolone. The biosynthesis of the acid takes place in the liver. Cholic acid is one of the four acids most commonly produced in the liver. The steroid plays a major role in cholesterol metabolism because of its emulsifying properties. The acid is transformed into bile salts in a biosynthesis, forming cholates. In the secondary form, cholic acid yields deoxycholic acid. Medicine uses cholic acid to dissolve gallstones and support liver health. Cholic acid participates in the enterohepatic circulation and is recycled more than ten times.
Anatomy and structure
Cholic acid is a colorless and crystalline substance with a bitter taste and a melting point of 198 degrees Celsius. The chemical molecular formula for the endogenous acid is C24H40O5. The substance is poorly soluble in water. It thus helps to mix substances that are actually immiscible and stabilizes these emulsions. Cholic acids are steroids from the sterol group, which belong to the lipid substance class. Their molecules form lipophilic groups. This means that they can easily dissolve fats and oils. Lipids are insoluble in water. They have a basic structure of four transconnected carbon rings. All bile acids of fat digestion consist of a hydrophobic and a hydrophilic part. Therefore, they can close around fats, allowing absorption of lipids in the gastrointestinal tract. In this context, cholic acid is particularly irreplaceable for the absorption of cholesterols.
Function and roles
During digestion, the fat-digesting enzyme lipase cleaves free fatty acids from lipids such as cholesterol ester. Lipases make available fats stored in the body and thus are also involved in the utilization of fats. Without the cleavage of free fatty acids, lipids would be indigestible for the body and could not be absorbed into the intestinal walls. To make the cleavage of free fatty acids more effective, lipids are stabilized in the gastrointestinal tract to form emulsions. Bile acids such as cholic acid act as emulsifiers in this process. In this way, they make the fats more accessible to lipases. This is preceded by the synthesis of cholic acid in the liver. Here, cholic acid is converted to glycocholic acid or glycine-cholic acid amide and taurocholic acid or taurine-cholic acid amide. These acids are transported into the bile. As salts, they enter the digestive system. When cholic acids have fulfilled their functions as emulsifiers, the small intestine reabsorbs them. More than 90 percent of acids are reabsorbed in secondary-active form by Na+ symport. About two percent are passively reabsorbed by nonionic and ionic diffusion in the small and large intestines. Through these resorption processes, only about three percent of cholic acids are released into the colon. Cytosolic transport proteins, together with anion exchangers, transport most of the cholic acid back through the basolateral membrane into the portal blood. In this way, cholic acids re-enter the liver. In the hepatocytes of the organ, they are conjugated and are once again available to the body. Only a fraction of cholic acid is lost daily in the stool. To compensate for these losses, the liver re-synthesizes a small amount of cholic acids day after day.
Diseases
When cholesterol breaks out of the emulsions of cholic acid, gallstones form. Thus, gallstone disease is a sign of a functional deficit of cholic acid. A deficiency of cholic acid can also cause gallstones, as this is another way in which the substance no longer fulfills its role in fat digestion. A cholic acid deficiency can have various causes. Congenital bile acid synthesis defects may be present.Even with chronic intestinal inflammation, however, there is no longer enough cholic acid, since cholic acid is no longer reabsorbed from inflamed areas in the small intestine. If cholic acid migrates daily in large quantities into the large intestine and is thus excreted in the stool, the closure valve separating the small intestine from the large intestine may be affected by inflammation or even a tumor. If chronic intestinal inflammation is the cause, the primary disease may correspond to the autoimmune disease Crohn’s disease. Liver diseases are just as likely to be responsible for a deficiency of cholic acid. For example, if the liver no longer synthesizes sufficient cholic acid, the daily losses via the stool cannot be adequately compensated for in the long term. Although the losses per day are minimal, they can add up in the long term and cause a general cholic acid deficiency. Such a deficiency is usually noticeable in a change in stool consistency. In particular, fatty stools refer to a deficiency of cholic acid, since fats can no longer be adequately adsorbed in the gastrointestinal tract in this deficiency condition and are thus excreted.
