- Joined
- Mar 5, 2014
- Messages
- 1,098
- Reaction score
- 102
why do alcoholics have reduced enterohepatic cycling of folate, and also with ileal disease you have decreased enterohepatic cycling, whats the reason?
In ileal disease there is decreased enterohepatic cycling of folate since folate is secreted into bile and reabsorbed in jejunum and ileum.@Transposony so let me get this straight, with ileal disease, you have decresed folate enterohepatic cycling(also seen in alcholism bc of decreases brush border conjugase activity) but with ileal disease you have increased Bilrubin enterhepatic cycling?
earlier you had mentioned bc of the GI conjugases which conjugate folate from the poly to the mono form. but rehardelss bilirubin cyclying is increased but folate is reduced. weird. with ileal disease still doestn make sense how you have increased bilirubin cycling but loss of bile acids.In ileal disease there is decreased enterohepatic cycling of folate since folate is secreted into bile and reabsorbed in jejunum and ileum.
The most important pathophysiology of pigment stone formation is increased amounts of unconjugated (insoluble) bilirubin in bile that precipitates (with calcium) to form stones.earlier you had mentioned bc of the GI conjugases which conjugate folate from the poly to the mono form. but rehardelss bilirubin cyclying is increased but folate is reduced. weird. with ileal disease still doestn make sense how you have increased bilirubin cycling but loss of bile acids.
Conjugation and solubilization are two different mechanisms. (see above)How can you solubilize unconjugated bilirubin in the colon? Isn't liver supposed to do that!
2. Ileal disease or resection → decreased bile salt absorption → relatively decreased bile salts in GB to solubilize unconjugated bilirubin ( from hydrolysis of conjugated bilirubin by endogenous β-glucuronidase) → precipitation of unconjugated bilirubin in the bile → pigment stone formation.