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Bile acid synthesis occurs in liver cells, which synthesize primary bile acids (cholic acid and chenodeoxycholic acid in humans) via cytochrome P450-mediated oxidation of cholesterol in a multi-step process. Approximately 600 mg of bile salts are synthesized daily to replace bile acids lost in the feces, although, as described below, much ...
Bile acid malabsorption was first recognized in patients with ileal disease. [22] When other causes were recognized, and an idiopathic, primary form described, [23] a classification into three types was proposed: [24] Type 1: Bile acid malabsorption, secondary to ileal resection, or ileal inflammation (e.g. in Crohn's disease)
The resulting imbalance between primary and secondary bile acids may lead to PSC via the gut-liver axis. [43] The primary bile acids cholic acid (CA) and chenodeoxycholic acid (CDCA) are synthesized in the liver and undergo conjugation before being released into the small intestine to aid digestion. [41]
Lactase deficiency inducing lactose intolerance (constitutional, secondary or rarely congenital) Intestinal disaccharidase deficiency; Intestinal enteropeptidase deficiency; Sucrose intolerance; Due to digestive failure. Bile acid/Bile salt malabsorption. Bacterial overgrowth; Obstructive jaundice; Primary bile acid diarrhea
Due to the pH of the small intestine, most of the bile acids are ionized and mostly occur as their sodium salts which are then called “primary conjugated bile salts.” In the lower small intestine and colon , bacteria dehydroxylate some of the primary bile salts to form secondary conjugated bile salts (which are still water-soluble).
It is metabolized by the enzyme 7α-hydroxycholest-4-en-3-one 12α-hydroxylase to 7α,12α-dihydroxycholest-4-en-3-one and then to cholic acid, the major primary bile acid in humans. Alternatively, it can be converted into 5β-cholestane-3α,7α-diol and then to chenodeoxycholic acid, the other major primary bile acid in humans. [1]
Secondary bile acids can influence innate immunity through their interactions with the bile acid receptors mentioned above, FXR and TGR-5. [19] FXR and TGR-5 are expressed by intestinal immune cells such as macrophages, as well as NKT cells and dendritic cells. [19] FXR has been shown to play a role with TLR-9 in inhibiting inflammation. [19 ...
Chimpanzee and human CYP3A4 are highly conserved in metabolism of many ligands, although four amino acids positively selected in humans led to a 5-fold benzylation of 7-BFC in the presence of the hepatotoxic secondary bile acid lithocholic acid. [12] This change in consequence contributes to an increased human defense against cholestasis. [12]