Long-term measurements of biliary cholesterol and bile acid secretion in the unanaesthetized mini-pig by controlled interruption of the enterohepatic circulation

1978 ◽  
Vol 173 (1) ◽  
pp. 55-66 ◽  
Author(s):  
W. Kaiser ◽  
K. Stocker ◽  
W. Erhardt
Keyword(s):  
Bile Acid ◽  
Acid Secretion ◽  
Enterohepatic Circulation ◽  
Biliary Cholesterol ◽  
Bile Acid Secretion

Bile Lipid Secretion in Obese and Non-Obese Individuals with and without Gallstones

1985 ◽  
Vol 69 (1) ◽  
pp. 71-79 ◽  
Author(s):  
A. Reuben ◽  
P. N. Maton ◽  
G. M. Murphy ◽  
R. H. Dowling
Keyword(s):  
Bile Acid ◽  
Acid Secretion ◽  
Biliary Lipid ◽  
Biliary Cholesterol ◽  
Cholesterol Gallstones ◽  
Lipid Secretion ◽  
Biliary Cholesterol Secretion ◽  
Cholesterol Secretion ◽  
Bile Acid Secretion ◽  
Secretion Rates

1. Biliary lipid secretion rates were measured in non-obese and obese individuals with and without cholesterol gallstones, using a steady-state, amino acid duodenal perfusion method. In addition, biliary lipid secretion rates were measured in five obese gallstone patients receiving high-dose chenodeoxycholic acid therapy (16-22 mg day−1 kg−1). 2. Bile acid secretion rates in the non-obese patients with cholesterol gallstones (563+sem 70 μmol/h, n = 6) were significantly lower than in the non-obese controls (1078 + 210 μmol/h, n = 10, P < 0.05), whereas cholesterol secretion rates were similar in the non-obese individuals with and without gallstones (51+7 and 42+4 μmol/h respectively). 3. In the obese, both with and without gallstones, the major abnormality was hypersecretion of cholesterol (107+7 μmol/h, n = 7, and 81 + 15 μmol/h, n = 7, respectively). Both these values were significantly greater than those in the non-obese controls (P < 0.01-0.02). 4. Biliary cholesterol secretion rates correlated significantly with bile acid secretion rates but, for every mole of bile acid secreted, the obese secreted more cholesterol than the non-obese. 5. Chenodeoxycholic acid treatment lowered biliary cholesterol saturation in obese gallstone patients by reducing biliary cholesterol secretion. 6. These results suggest that there are two major types of defect in biliary lipid secretion in gallstone patients: reduced biliary bile acid secretion in non-obese gallstone patients and excessive biliary cholesterol secretion in the obese.

scholarly journals Bile acid secretion by cultured rat hepatocytes. Regulation by cholesterol availability.

1983 ◽  
Vol 258 (6) ◽  
pp. 3661-3667 ◽  
Author(s):  
R A Davis ◽  
P M Hyde ◽  
J C Kuan ◽  
M Malone-McNeal ◽  
J Archambault-Schexnayder
Keyword(s):  
Bile Acid ◽  
Acid Secretion ◽  
Rat Hepatocytes ◽  
Cultured Rat Hepatocytes ◽  
Bile Acid Secretion

Aluminum Trichloride Disorders Bile Acid Secretion and Induces Hepatocyte Apoptosis in Rats

2015 ◽  
Vol 71 (3) ◽  
pp. 1569-1577 ◽  
Author(s):  
Yue She ◽  
Hansong Zhao ◽  
Yanzhu Zhu ◽  
Yanfei Han ◽  
Shiliang Xia ◽  
...  
Keyword(s):  
Bile Acid ◽  
Acid Secretion ◽  
Hepatocyte Apoptosis ◽  
Aluminum Trichloride ◽  
Bile Acid Secretion

Differing effects of norcholate and cholate on bile flow and biliary lipid secretion in the rat

1984 ◽  
Vol 246 (1) ◽  
pp. G67-G71
Author(s):  
E. R. O'Maille ◽  
S. V. Kozmary ◽  
A. F. Hofmann ◽  
D. Gurantz
Keyword(s):  
Bile Acid ◽  
Acid Secretion ◽  
Bile Acids ◽  
Bile Flow ◽  
Critical Micellar Concentration ◽  
Biliary Lipid ◽  
Lipid Secretion ◽  
Unit Increase ◽  
Cholesterol Secretion ◽  
Bile Acid Secretion

The effects of norcholate (a C23 bile acid that differs from cholate in having a side chain containing four rather than five carbon atoms) on bile flow and biliary lipid secretion were compared with those of cholate, using the anesthetized rat with a bile fistula. Norcholate and cholate were infused intravenously over the range of 0.6-6.0 mumol X min-1 X kg-1. Both bile acids were quantitatively secreted into bile; norcholate was secreted predominantly in unconjugated form in contrast to cholate, which was secreted predominantly as its taurine or glycine conjugates. The increase in bile flow per unit increase in bile acid secretion induced by norcholate infusion [17 +/- 3.2 (SD) microliters/mumol, n = 8] was much greater than that induced by cholate infusion (8.6 +/- 0.9 microliters/mumol, n = 9) (P less than 0.001). Both bile acids induced phospholipid and cholesterol secretion. For an increase in bile acid secretion (above control values) of 1 mumol X min-1 X kg-1, the increases in phospholipid secretion [0.052 +/- 0.024 (SD) mumol X min-1 X kg-1, n = 9] and cholesterol secretion (0.0071 +/- 0.0033 mumol X min-1 X kg-1, n = 9) induced by norcholate infusion were much less than those induced by cholate infusion (0.197 +/- 0.05 mumol X min-1 X kg-1, n = 9, and 0.024 +/- 0.011 mumol X min-1 X kg-1, n = 9, respectively; P less than 0.001 for both phospholipid and cholesterol). The strikingly different effects of norcholate on bile flow and biliary lipid secretion were attributed mainly to its possessing a considerably higher critical micellar concentration than cholate.

scholarly journals Metabolic consequences of ileal interruption of the enterohepatic circulation of bile acids

2020 ◽  
Vol 319 (5) ◽  
pp. G619-G625
Author(s):  
Ivo P. van de Peppel ◽  
Henkjan J. Verkade ◽  
Johan W. Jonker
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Enterohepatic Circulation ◽  
Current Knowledge ◽  
Whole Body ◽  
Novel Studies ◽  
Sodium Dependent ◽  
Bile Acid Transporter ◽  
Bile Acid Secretion ◽  
Different Levels

The enterohepatic circulation of bile acids comprises a tightly regulated process of hepatic bile acid secretion, intestinal reabsorption and transport back to the liver. Disruption of this process has significant consequences for gastrointestinal, liver and whole body homeostasis and therefore offers opportunities for therapeutic intervention. In this review we discuss the effects of (pharmacological) interruption of the enterohepatic circulation at different levels. Recently, several studies have been published on ileal interruption of the enterohepatic circulation of bile acids, targeting the apical-sodium dependent bile acid transporter (ASBT, SLC10A2), as therapy for various diseases. However, ambiguous results have been reported and in-depth mechanistic insights are lacking. Here we discuss these novel studies and review the current knowledge on the consequences of ASBT inhibition and its potential effects on physiology and metabolism.

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