The effect of dietary cholesterol on bile acid synthesis in rat liver

1985 ◽  
Vol 13 (5) ◽  
pp. 873-874 ◽  
Author(s):  
KATHLEEN M. BOTHAM ◽  
GEORGE S. BOYD
1992 ◽  
Vol 40 (2) ◽  
pp. 446-448 ◽  
Author(s):  
Yasumasa KOIBUCHI ◽  
Junji YAMADA ◽  
Takafumi WATANABE ◽  
Takao KUROSAWA ◽  
Sadahiko TOHMA ◽  
...  

1980 ◽  
Vol 103 (2) ◽  
pp. 299-305 ◽  
Author(s):  
Kathleen M. BOTHAM ◽  
Geoffrey J. BECKETT ◽  
Iain W. PERCY-ROBB ◽  
George S. BOYD

1985 ◽  
Vol 230 (1) ◽  
pp. 19-24 ◽  
Author(s):  
H Seltman ◽  
W Diven ◽  
M Rizk ◽  
B J Noland ◽  
R Chanderbhan ◽  
...  

Sterol carrier protein2 (SCP2) is known to stimulate utilization of cholesterol in enzymic reactions in which cholesterol is the substrate. Substantial recent experimental evidence indicates that SCP2: activates enzymic conversion of intermediates between lanosterol and cholesterol; stimulates the microsomal conversion of cholesterol into cholesterol ester in rat liver; and enhances mitochondrial utilization of cholesterol for pregnenolone formation in the adrenals. The conversion of cholesterol into 7 α-hydroxycholesterol is the rate-limiting step in bile-acid synthesis. We therefore investigated the effect of SCP2 on this physiologically critical reaction by using a gas-chromatography-mass-spectrometry procedure that measures the mass of 7 α-hydroxycholesterol formed. The results show that SCP2 enhances 7 α-hydroxycholesterol formation by rat liver microsomes (microsomal fractions), utilizing either endogenous membrane cholesterol, cholesterol supplied exogenously in serum or in the form of cholesterol/phospholipid liposomes. Microsomes immunotitrated with anti-SCP2 antibody exhibited considerably less capacity to synthesize 7 α-hydroxycholesterol, which was restored to control levels on addition of purified SCP2. These data are consistent with the suggestion that SCP2 may be of physiological significance in the overall metabolism of cholesterol.


1979 ◽  
Vol 178 (1) ◽  
pp. 71-78 ◽  
Author(s):  
R C Strange ◽  
G J Beckett ◽  
I W Percy-Robb

1. Normally fed and cholestyramine-treated rats were injected through the superior mesenteric vein with different amounts of radiolabelled glycoholic acid and the appearance of radioactivity in bile was measured. 2. In normally fed rats radioactivity appeared in bile within 30 s of injection and reached a maximum after 2 1/2 min; in the cholestyramine-treated animals the appearance of radioactivity was slower and less of the injected material was excreted into bile. 3. At 10 min after injection, livers were removed and the amounts of radioactive glycoholic acid and endogenous cholic acid conjugates in nuclei and cytosol were determined; most of the bile acid was found in the cytosol, only small amounts being found in nuclei. 4. Nuclear preparations from both normally fed and cholestyramine-fed rats were extracted with KCl (0.4 M) in an attempt to identify a putative bile acid receptor, but no such receptor was found. 5. Regulation of bile acid synthesis does not involve nuclear binding of bile acids.


1991 ◽  
Vol 276 (1) ◽  
pp. 73-77 ◽  
Author(s):  
B Ugele ◽  
H J M Kempen ◽  
R Gebhardt ◽  
P Meijer ◽  
H J Burger ◽  
...  

Periportal and perivenous hepatocytes were isolated from rat liver by digitonin/collagenase perfusion for investigating the acinar distribution of bile acid synthesis. The specific activity of cholesterol 7 alpha-hydroxylase (EC 1.14.13.17) was 7.9-fold higher in perivenous cells than in periportal hepatocytes. Mass production of bile acids differed 4.4-fold between cultured perivenous and periportal hepatocytes. In contrast, the levels of free cholesterol in homogenates and microsomes derived from both subfractions were similar. Feeding of rats with the bile-acid-sequestering anion-exchange resin colestid resulted in a pronounced stimulation of cholesterol 7 alpha-hydroxylase activity and bile acid mass production, but decreased the perivenous/periportal ratio of both parameters. These results demonstrate that bile acid mass production, but decreased the perivenous hepatocytes, possibly owing to feedback suppression by bile acids from the enterohepatic circulation. Furthermore, the opposite acinar localization of cholesterol and bile acid biosynthesis provides an interesting alternative to current views of the regulation of their metabolic pathways.


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.


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