Influence of bile acids on biliary lipid excretion in man

1968 ◽  
Vol 13 (12) ◽  
pp. 1077-1080 ◽  
Author(s):  
Leon Swell ◽  
C. C. Bell
Keyword(s):  
Bile Acids ◽  
Biliary Lipid ◽  
Lipid Excretion

Faecal Lipid Excretion Levels in Normal Japanese Females on an Unrestricted Diet and a Fat-Restricted Diet Measured by Simultaneous Analysis of Faecal Lipids

1992 ◽  
Vol 20 (6) ◽  
pp. 461-466 ◽  
Author(s):  
T Nakamura ◽  
H Kikuchi ◽  
K Takebe ◽  
K Kudoh ◽  
A Terada ◽  
...  
Keyword(s):  
Bile Acids ◽  
Dietary Fat ◽  
Chromatographic Method ◽  
Simultaneous Analysis ◽  
Restricted Diet ◽  
Neutral Sterol ◽  
Neutral Sterols ◽  
Unrestricted Diet ◽  
Lipid Excretion ◽  
Normal Japanese

Faecal lipid excretion was determined in 16 females on an unrestricted diet and on a fat-restricted diet using a chromatographic method for the simultaneous analysis of faecal lipids. The fat-restricted diet reduced the total quantity of faeces and the amounts of fatty acids, neutral sterols and bile acids excreted were almost halved compared with when on an unrestricted diet. This indicates that dietary fat, fibre and cholesterol affect the amount of faecal bile acid, neutral sterol and fatty acid excretion. The amount of cholesterol/animal sterols excreted and the percentage of primary bile acids were, however, similar for both the fat-restricted and unrestricted diets.

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 Changes in Biliary Lipid Concentrations in Bile Duct Obstruction: An Experimental Study

1986 ◽  
Vol 79 (9) ◽  
pp. 522-527 ◽  
Author(s):  
Xu Guorong ◽  
C J C Kirk ◽  
A W Goode
Keyword(s):  
Experimental Study ◽  
Bile Duct ◽  
Bile Acids ◽  
Significant Role ◽  
Biliary Obstruction ◽  
Enterohepatic Circulation ◽  
Biliary Lipid ◽  
Complete Obstruction ◽  
Duct Obstruction ◽  
Biliary Lipids

Changes in biliary concentrations of bile acids, phospholipids and cholesterol and biliary pressures were measured in dogs. These parameters were studied during 7-day periods of partial biliary obstruction, of varying degrees, and after 24-hour and 48-hour periods of complete obstruction. The samples were obtained via an exteriorized but intact enterohepatic circulation allowing the introduction of varying degrees of obstruction and bile sampling. Biliary obstruction reduced the concentration of all biliary lipids especially when the obstruction produced pressures in excess of 75% of the maximum biliary secretion pressure. Only immediately after the release of a 48-hour period of complete obstruction did the risk of cholesterol supersaturation of bile occur. However, at that time there was a greatly reduced concentration of lipids in the bile and the amount of cholesterol that could potentially have precipitated was very small. It is suggested that this supersaturation would not play a significant role in the formation of gallstones.

Effect of primary bile acids on bile lipid secretion from perfused dog liver

1975 ◽  
Vol 229 (3) ◽  
pp. 714-720 ◽  
Author(s):  
NE Hoffman ◽  
DE Donald ◽  
AF Hosmann
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Liver Perfusion ◽  
Biliary Lipid ◽  
Hepatic Extraction ◽  
Perfusion Technique ◽  
Lipid Secretion ◽  
Cholesterol Secretion ◽  
Dog Liver ◽  
Bile Acid Secretion

An isolated canine liver perfusion technique featuring a second dog as the pump oxygenator was used to compare biliary lipid secretion during randomized, steady-state perfusions at two different rates of cholyl taurine or chenodeoxycholyl taurine infusions. The hepatic extraction of the trihydroxy-conjugated bile acid was considerably greater than that of the dihydroxy conjugate, possibly explained by ultrafiltration experiments which indicated that cholyl taurine was less protein bound than chenodeoxycholyl taurine. Both bile acids induced phospholipid and cholesterol secretion that was linearly proportional to bile acid secretion. However, each mole of secreted chenodeoxycholyl taurine induced a greater relative secretion of phospholipid and cholesterol than did that of cholyl taurine. Thus in the canine liver, the two primary bile acids are extracted at different rates and induce biliary secretion of different relative lipid composition.

Determinants of Biliary Lipid Excretion

2015 ◽  
pp. 368-375
Author(s):  
H. O. Wheeler ◽  
R. J. May ◽  
P. M. Loeb
Keyword(s):  
Biliary Lipid ◽  
Lipid Excretion

Bile Acids and Lipid Metabolism. I. Stimulation of Bile Lipid Excretion by Various Bile Acids

1968 ◽  
Vol 127 (4) ◽  
pp. 1003-1006 ◽  
Author(s):  
C. Entemnan ◽  
R. J. Holloway ◽  
M. L. Albright ◽  
G. F. Leong
Keyword(s):  
Lipid Metabolism ◽  
Bile Acids ◽  
Lipid Excretion ◽  
Stimulation Of

Hepatic and ileal transport and effect on biliary secretion of norursocholic acid and its conjugates in rats

1991 ◽  
Vol 261 (6) ◽  
pp. G1057-G1064
Author(s):  
J. Lillienau ◽  
L. R. Hagey ◽  
B. Borgstrom
Keyword(s):  
Bile Acids ◽  
Bile Flow ◽  
Enterohepatic Circulation ◽  
Biliary Lipid ◽  
Perfusion Technique ◽  
Hepatic Transport ◽  
Rate Of Absorption ◽  
Cholesterol Secretion ◽  
Hepatic Biotransformation

The enterohepatic circulation of norursocholic acid (nUC) and its glycine (nUCG) and taurine (nUCT) conjugates was investigated in the rat; cholic acid (C) was studied as control. The biliary recovery of intravenously infused 14C-labeled bile acids was high: nUC, 88%; nUCG, 80%; nUCT, 99%, and C, 90%. Biliary recovery after the same bile acids were infused intraduodenally was similar: nUC, 90%; nUCG, 66%; nUCT, 97%; and C, 99%. The two conjugated bile acids, nUCG and nUCT, were not biotransformed during intestinal or hepatic transport; nUC was also secreted largely unchanged, but approximately 10% was secreted as an unknown conjugate or sulfate; C was completely conjugated with taurine or glycine. To compare the rates of active ileal transport, biliary recovery was measured after an in situ ileal perfusion technique. The rate of absorption of nUC, nUCG, and nUCT was one-fourth to one-half that of cholyltaurine, which served as control. Competition experiments indicated that the same transport system was involved. When infused intravenously, nUC, nUCG, and nUCT induced far less biliary lipid secretion than an identical dose of C; the secretion of both phospholipid and cholesterol was decreased, cholesterol to a greater extent than phospholipid. It is concluded that nUC and its conjugates are well transported by the ileum, are efficiently secreted into bile without undergoing appreciable hepatic biotransformation, and induce bile flow as other hydrophilic bile acids, but in contrast to C induce little phospholipid and cholesterol secretion into bile.

Lack of biliary lipid excretion in the little skate, Raja erinacea, indicates the absence of functional Mdr2, Abcg5, and Abcg8 transporters

2004 ◽  
Vol 286 (5) ◽  
pp. G762-G768 ◽  
Author(s):  
Ronald P. J. Oude Elferink ◽  
Roelof Ottenhoff ◽  
Gert Fricker ◽  
David J. Seward ◽  
Nazzareno Ballatori ◽  
...  
Keyword(s):  
Bile Salt ◽  
Plasma Membranes ◽  
Biliary Tree ◽  
Biliary Lipid ◽  
Raja Erinacea ◽  
P Glycoprotein ◽  
Primitive Species ◽  
Cholesterol Excretion ◽  
Current Paradigm ◽  
Lipid Excretion

The ABC transporters bile salt export pump (BSEP; encoded by the ABCB11 gene), MDR3 P-glycoprotein ( ABCB4), and sterolin 1 and 2 ( ABCG5 and ABCG8) are crucial for the excretion of bile salt, phospholipid, and cholesterol, respectively, into the bile of mammals. The current paradigm is that phospholipid excretion mainly serves to protect membranes of the biliary tree against bile salt micelles. Bile salt composition and cytotoxicity, however, differ greatly between species. We investigated whether biliary phospholipid and cholesterol excretion occurs in a primitive species, the little skate, which almost exclusively excretes the sulphated bile alcohol scymnolsulphate. We observed no phospholipid and very little cholesterol excretion into bile of these animals. Conversely, when scymnolsulphate was added to the perfusate of isolated mouse liver perfusions, it was very well capable of driving biliary phospholipid and cholesterol excretion. Furthermore, in an erythrocyte cytolysis assay, scymnolsulphate was found to be at least as cytotoxic as taurocholate. These results demonstrate that the little skate does not have a system for the excretion of phospholipid and cholesterol and that both the MDR3 and the two half-transporter genes, ABCG5 and ABCG8, have evolved relatively late in evolution to mediate biliary lipid excretion. Little skate plasma membranes may be protected against bile salt micelles mainly by their high sphingomyelin content.

Taurocholate induces pericanalicular localization of C6-NBD-ceramide in isolated hepatocyte couplets

1991 ◽  
Vol 260 (1) ◽  
pp. G119-G132 ◽  
Author(s):  
J. M. Crawford ◽  
D. W. Vinter ◽  
J. L. Gollan
Keyword(s):  
Golgi Apparatus ◽  
Biliary Excretion ◽  
Digital Image Analysis ◽  
Perfused Liver ◽  
Biliary Lipid ◽  
Rat Hepatocyte ◽  
Intracellular Organelles ◽  
Microscopic Findings ◽  
Lipid Excretion ◽  
Fluorescent Lipid

The mechanisms and pathways involved in hepatocellular transport of lipid destined for biliary excretion remain poorly understood. Using fluorescence microscopy of rat hepatocyte couplets in primary culture, we examined the effects of taurocholate (TC) on the intracellular distribution of 6-N-[7-nitrobenz-2-oxa-1,3-diazol- 4-yl]aminocaproyl-sphingosine (C6-NBD-ceramide), a lipid that accumulates in the Golgi apparatus. Microscopic findings were quantified with morphometric and digital image analysis and were correlated with the metabolism of C6-NBD-ceramide in isolated hepatocyte suspensions and the biliary excretion of fluorescent lipid in the isolated perfused liver. After plasma membrane uptake of C6-NBD-ceramide from albumin at 0 degrees C, the lipid was rapidly internalized at 37 degrees C but exhibited only a modest concentration of fluorescence in intracellular organelles. With 17 microM TC in the medium, there was enhanced localization of fluorescence to organelles and significant recruitment of fluorescent lipid to the pericanalicular region of the couples within 30 min. C6-NBD-ceramide was partially metabolized to C6-NBD-sphingomyelin and -glucosylceramide, indicative of transit through the Golgi apparatus. The generation of C6-NBD-sphingomyelin was significantly increased by TC. After a similar loading protocol in the perfused liver, there was little biliary excretion of fluorescent lipid at 37 degrees C under control conditions. However, infusion of TC markedly enhanced the biliary output of fluorescent lipid over the first 30 min, primarily as C6-NBD-sphingomyelin and -glucosylceramide. We conclude that TC modulates the distribution of C6-NBD-ceramide in hepatocytes by inducing translocation of lipid to a pericanalicular location, most likely the Golgi apparatus, before excretion of its metabolites in bile. Our findings support the concept that bile salt-induced biliary lipid excretion is facilitated by the interaction of bile salts with lipids at the level of intracellular organelles.

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