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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)
Bile acids also have hormonal actions throughout the body, particularly through the farnesoid X receptor and GPBAR1 (also known as TGR5). [1] [3] Bile acid synthesis is the only manner in which humans or other mammals may excrete excess cholesterol, as the parent compound of all bile acids is cholesterol. [1]
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).
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
The resulting imbalance between primary and secondary bile acids may lead to PSC via the gut-liver axis. [44] 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. [42]
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]
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 ...
20493 Ensembl ENSG00000100652 ENSMUSG00000021135 UniProt Q14973 O08705 RefSeq (mRNA) NM_003049 NM_001177561 NM_011387 NM_001361972 RefSeq (protein) NP_003040 NP_001171032 NP_035517 NP_001348901 Location (UCSC) Chr 14: 69.78 – 69.8 Mb Chr 12: 81 – 81.02 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Sodium/bile acid cotransporter also known as the Na + - taurocholate ...