THU-004-Lactobacillus rhamnosus GG prevents liver fibrosis through intestinal FXR/FGF15-mediated inhibition of bile acid synthesis and the increase of bile acid excretion in mice

2019 ◽  
Vol 70 (1) ◽  
pp. e162-e163
Author(s):  
Wenke Feng ◽  
Yunhuan Liu ◽  
Craig McClain
1962 ◽  
Vol 203 (6) ◽  
pp. 1029-1032 ◽  
Author(s):  
Jean D. Wilson

The influence of dietary cholesterol on fecal excretion of bile acids has been studied in rats fed isocaloric quantities of purified diets that varied only in cholesterol content. Addition of dietary cholesterol clearly resulted in an increase in excretion of total bile acids, as well as in conversion of cholesterol-4-C14 to bile acid-C14. An acceleration in bile acid excretion as a result of cholesterol feeding was demonstrated to be independent of dietary cholic acid and to occur despite suppression of the bowel flora. These results suggest that not only does absorbed dietary cholesterol play a role in determining the rate of bile acid formation but that the adaptation of bile acid synthesis to cholesterol feeding may in part be a determining factor in the varying response of different species to cholesterol feeding.


2016 ◽  
Vol 113 (40) ◽  
pp. 11289-11293 ◽  
Author(s):  
Sílvia Vilarinho ◽  
Sinan Sari ◽  
Francesca Mazzacuva ◽  
Kaya Bilgüvar ◽  
Güldal Esendagli-Yilmaz ◽  
...  

Acyl CoA Oxidase 2 (ACOX2) encodes branched-chain acyl-CoA oxidase, a peroxisomal enzyme believed to be involved in the metabolism of branched-chain fatty acids and bile acid intermediates. Deficiency of this enzyme has not been described previously. We report an 8-y-old male with intermittently elevated transaminase levels, liver fibrosis, mild ataxia, and cognitive impairment. Exome sequencing revealed a previously unidentified homozygous premature termination mutation (p.Y69*) in ACOX2. Immunohistochemistry confirmed the absence of ACOX2 expression in the patient’s liver, and biochemical analysis showed marked elevation of intermediate bile acids upstream of ACOX2. These findings define a potentially treatable inborn error of bile acid biosynthesis caused by ACOX2 deficiency.


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