Enterohepatic circulation of<unk>  salts<unk> <unk> s (also called<unk>  salts) are produced in the liver, secreted into the biliary system, stored in the gallbladder and are released after meals stimulated by cholecystokinin. They are important for the digestion and absorption of fats (lipids) in the small intestine. Usually over 95% of the<unk> <unk> s are absorbed in the terminal ileum and are taken up by the liver and resecreted. This enterohepatic circulation of<unk> <unk> s takes place 4-6 times in 24 hours and usually less than 0.5 g of<unk> <unk> s enter the large intestine per 24 h. When larger amounts of<unk> <unk> s enter the large intestine, they stimulate water secretion and intestinal motility in the colon, which causes symptoms of chronic diarrhea. Intestinal absorption of<unk> <unk> s The ileum is very efficient at absorbing the glyco- and taurine-conjugated forms of the<unk>  salts. The apical sodium-dependent<unk>  salt transporter (ASBT, IBAT, gene symbol SLC10A2) is the first step in absorption at the brush-border membrane. The cytoplasmic ileal<unk> <unk>  binding protein (IBABP, ILBP, gene symbol FABP6) and the basolateral heterodimer of OSTα and OSTβ transfer<unk> <unk> s through and out of the cell where they eventually enter the portal vein. These<unk> <unk>  transporters are all highly expressed in the ileum but not in the liver, jejunum or colon. When expression of these specialized transporters is reduced, the intestine is less efficient at<unk> <unk>  reabsorption (Type 1<unk> . If intestinal motility is affected by gastro-intestinal surgery, or<unk> <unk> s are deconjugated by small intestinal bacterial overgrowth, absorption is less efficient (Type 3<unk> . A very small proportion of the patients with no obvious disease (Type 2<unk>  may have mutations in ASBT, but this mutation is not more common in most patients and does not affect function. Overproduction of<unk> <unk> s Primary<unk> <unk>  diarrhea (Type 2<unk> ") may be caused by an overproduction of<unk> <unk> s. Several groups of workers have failed to show any defect in ileal<unk> <unk>  absorption in these patients, and they have an enlarged<unk> <unk>  pool, rather than the reduced pool expected with<unk> . The synthesis of<unk> <unk> s in the liver is negatively regulated by the ileal hormone fibroblast growth factor 19 (FGF19), and lower levels of this hormone result in overproduction of<unk> <unk> s, which are more than the ileum can absorb.
Bile acid malabsorption
Irritable bowel syndrome
Fructose malabsorption
Microscopic colitis
Glucose-galactose malabsorption
Exocrine pancreatic insufficiency
Sucrose intolerance
Lactose intolerance