Influence of bile salts and lipids on intestinal absorption of griseofulvin in man

1986 ◽  
Vol 31 (3) ◽  
pp. 319-325 ◽  
Author(s):  
R. Palma ◽  
N. Vidon ◽  
G. Houin ◽  
A. Pfeiffer ◽  
M. Rongier ◽  
...  
1977 ◽  
Vol 25 (8) ◽  
pp. 1974-1979 ◽  
Author(s):  
RYOHEI HORI ◽  
KATSUHIKO OKUMURA ◽  
KENICHI INUI ◽  
NOBUKUNI NAKAMURA ◽  
AKIMA MIYOSHI ◽  
...  

1967 ◽  
Vol 46 (1) ◽  
pp. 164-168 ◽  
Author(s):  
O.B. Lindsay ◽  
B.E. March

1976 ◽  
Vol 24 (9) ◽  
pp. 2014-2020 ◽  
Author(s):  
KIKUO IWAMOTO ◽  
NORIKO OZAWA ◽  
FUMIE ITO ◽  
NORIKO OKAMOTO ◽  
JUN WATANABE

1980 ◽  
Vol 58 (9) ◽  
pp. 1058-1062 ◽  
Author(s):  
Ch. Marteau ◽  
M. O. Reynier ◽  
C. Crotte ◽  
A. Mule ◽  
S. Mathieu ◽  
...  

After this time, the cholesterol intestinal absorption and the biliary secretion of lipids were measured. The biliary secretion of cholesterol, the total hepatic cholesterol (23 mg/g liver dry weight), and the intestinal absorption of cholesterol (90% administered dose) were higher in mice fed with cholic acid than in mice fed with chenodeoxycholic acid (hepatic cholesterol, 9.6 mg/g liver dry weight; absorption, 65% administered dose).The addition of β-sitosterol to the diet supplemented with cholic acid decreased the cholesterol intestinal absorption and the biliary secretion of cholesterol so that both became similar to that obtained with chenodeoxycholic acid.These results indicate that in mice, as in man, cholic acid elicits a higher cholesterol biliary secretion than chenodeoxycholic acid. In this experimental model, the distinct effect on the biliary cholesterol of these two bile salts is due to their specific effects on the intestinal absorption of cholesterol.


1979 ◽  
Vol 94 (3) ◽  
pp. 472-476 ◽  
Author(s):  
R.C. de Belle ◽  
V. Vaupshas ◽  
B.B. Vitullo ◽  
L.R. Haber ◽  
E. Shaffer ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245302
Author(s):  
Felice Amato ◽  
Alice Castaldo ◽  
Giuseppe Castaldo ◽  
Gustavo Cernera ◽  
Gaetano Corso ◽  
...  

This study aims to investigate cholesterol metabolism in a mouse model with cystic fibrosis (CF) by the comparison of affected homozygous versus wild type (WT) mice. In particular, we evaluated the effects of a diet enriched with cholesterol in both mice groups in comparison with the normal diet. To this purpose, beyond serum and liver cholesterol, we analyzed serum phytosterols as indirect markers of intestinal absorption of cholesterol, liver lathosterol as indirect marker of de novo cholesterol synthesis, liver cholestanol (a catabolite of bile salts synthesis) and the liver mRNA levels of LDL receptor (LDLR), 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoAR), acyl CoA:cholesterol acyl transferase 2 (ACAT2), cytochrome P450 7A1 (CYP7A1) and tumor necrosis factor alpha (TNFα). CF mice showed lower intestinal absorption and higher liver synthesis of cholesterol than WT mice. In WT mice, the cholesterol supplementation inhibits the synthesis of liver cholesterol and enhances its catabolism, while in CF mice we did not observe a reduction of LDLR and HMG-CoAR expression (probably due to an altered feed-back), causing an increase of intracellular cholesterol. In addition, we observed a further increase (5-fold) in TNFα mRNA levels. This preliminary study suggests that in CF mice there is a vicious circle in which the altered synthesis/secretion of bile salts may reduce the digestion/absorption of cholesterol. As a result, the liver increases the biosynthesis of cholesterol that accumulates in the cells, triggering inflammation and further compromising the metabolism of bile salts.


2013 ◽  
Vol 452 (1-2) ◽  
pp. 374-381 ◽  
Author(s):  
Zhiwen Zhang ◽  
Fang Gao ◽  
Shijun Jiang ◽  
Lingli Chen ◽  
Zeying Liu ◽  
...  

1985 ◽  
Vol 248 (6) ◽  
pp. G718-G725
Author(s):  
M. D. Sitrin ◽  
K. L. Pollack ◽  
M. J. Bolt

Intestinal absorption of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] from in vivo jejunal sacs was studied in rats with thoracic duct and bile duct cannulas. In 6 h 86.5% of the administered 1,25(OH)2D3 was absorbed, but only 7.3% was recovered in thoracic duct lymph. Appearance in plasma of [3H]-1,25(OH)2D3 after intrajejunal administration was identical in rats with and without diverting lymph cannulas, indicating that the 1,25(OH)2D3 is absorbed almost entirely via portal blood. When 1,25(OH)2D3 was instilled into the jejunum in a fat suspension without bile salts rather than a mixed micellar solution, less was recovered in lymph, but total intestinal absorption was unchanged. High-pressure liquid chromatography of a lymph extract demonstrated that 1,25(OH)2D3 was present only as the unchanged secosteroid. In lymph, only 4.1% of the 1,25(OH)2D3 was in the chylomicrons, with the remainder bound to the plasma protein fraction of lymph. Treatment of rats with cycloheximide to block chylomicron synthesis did not decrease absorption of 1,25(OH)2D3. These results indicate that intestinal absorption of 1,25(OH)2D3 is effective and not very dependent on luminal bile salts. Almost all 1,25(OH)2D3 is released from the intestine directly into portal blood and does not require packaging in chylomicrons for transport into intestine lymph.


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