Erythritol and mannitol clearances with taurocholate and secretin-induced cholereses.

1978 ◽  
Vol 234 (2) ◽  
pp. E146
Author(s):  
J L Barnhart ◽  
B Combes
Keyword(s):  
Bile Flow ◽  
Total Concentration ◽  
Sodium Taurocholate ◽  
Fixed Amount ◽  
Bile Formation ◽  
Canalicular Bile ◽  
Wide Range ◽  
Bile Production ◽  
Mean Concentration ◽  
Erythritol And Mannitol

The biliary clearances of [14C]erythritol (Cery) and [3H]mannitol (Cmann) were measured simultaneously in dogs during cholereses induced by sodium taurocholate and by secretin. Cery increased equally with the increase in bile flow induced by taurocholate, whereas mannitol entry into bile was partially restricted; deltaCery/deltabile flow averaged 0.96; deltaCmann/deltaCery averaged 0.81. Values for erythritol clearance exceeded bile flow by a constant volume over a wide range of bile flows, a result that suggests distal reabsorption of a fixed amount of fluid, independent of canalicular bile production. During secretin-induced choleresis both Cery and Cmann accompanied 30-40% of the increase in bile flow, and the ratio of Cmann/Cery was 1.02. Thus the secretin-responsive region is permeable to both erythritol and mannitol. This affects the extent to which measured erythritol clearance accurately reflects canalicular bile formation; Cery may underestimate or overestimate canalicular bile flow. The electrolyte composition of bile remained relatively constant over a broad range of bile flows although the characteristics of taurocholate- and secretin-induced biles differed from each other. Taurocholate-stimulated bile was virtually isotonic. Secretin-induced bile had a high total concentration of electrolyte (mean concentration 367 meq/liter) rich in chloride and bicarbonate and was hypertonic.

[14C]erythritol clearance and canalicular bile acid-independent flow in the baboon

1982 ◽  
Vol 242 (5) ◽  
pp. G475-G480
Author(s):  
S. M. Strasberg ◽  
R. G. Ilson ◽  
C. N. Petrunka
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Bile Flow ◽  
Quantitative Assessment ◽  
Sodium Taurocholate ◽  
Hepatic Bile ◽  
Bile Formation ◽  
Canalicular Bile

The use of [14C]erythritol for the quantitative assessment of hepatic bile formation has been studied in baboons using sodium taurocholate to generate canalicular bile flow. It has been found that increments in [14C]erythritol clearance are equal to taurocholate-induced increments in bile flow, but there was no change in [14C]erythritol clearance when bile flow was increased by secretin. No evidence was found to support the view that bile acids affect bile acid-independent bile flow.

Effect of protoporphyrin IX on ursodeoxycholate-induced hypercholeresis in the rat

1988 ◽  
Vol 75 (6) ◽  
pp. 593-599
Author(s):  
J. J. Garcia-Marin ◽  
J. G. Redondo-Torres ◽  
F. Perez-Barriocanal ◽  
M. M. Berenson
Keyword(s):  
Body Weight ◽  
Bile Acid ◽  
Bile Flow ◽  
Sodium Taurocholate ◽  
Protoporphyrin Ix ◽  
Inhibitory Effect ◽  
Bicarbonate Secretion ◽  
Bile Formation ◽  
Dose Dependent ◽  
Bile Acid Secretion

1. It is known that the perfusion of rat livers with solutions containing protoporphyrin IX induces a decrease in bile flow which is not due to inhibition of bile acid secretion but rather to decreased electrolyte transport into bile. By contrast, ursodeoxycholate induces hypercholeresis, partly due to a marked stimulation of biliary bicarbonate secretion. The aim of the present work was to investigate the effect of protoporphyrin IX on ursodeoxycholate-induced choleresis in anaesthetized male Wistar rats. 2. Protoporphyrin IX infusion at rates of 10, 20 and 40 μg min−1 100 g−1 body weight into the jugular vein induced a dose-dependent inhibitory effect on bile flow as well as on bile acid and electrolyte secretion. The lowest infused rate only induced slight and non-significant changes in spontaneous bile formation and functional variables such as glycaemia, packed cell volume, blood pH, Pco2, Po2 and bicarbonate concentration, and in hepatic carbonic anhydrase activity. It was thus considered as a subtoxic dose. 3. Sodium taurocholate was infused (0.5 μmol min−1 100 g−1 body weight) over the second hour of the lowest dose of protoporphyrin IX infusion. In these rats, no significant changes in bile flow or bile acid and electrolyte secretion were observed as compared with animals receiving sodium taurocholate plus saline solution. 4. Bile acid secretion induced by ursodeoxycholate infusion (1 μmol min−1 100 g−1 body weight) was similar both in rats receiving ursodeoxycholate plus saline solution and in animals infused with this bile acid over the second hour of the lowest dose of protoporphyrin IX infusion. However, bile flow and biliary bicarbonate secretion induced by ursodeoxycholate were markedly impaired (− 43% and − 56%, respectively) by protoporphyrin IX. 5. These results indicate that in the rat, in vivo, protoporphyrin IX impairs bile formation in a dose-dependent manner. They suggest that the mechanism(s) involved in ursodeoxycholate-induced bicarbonate secretion, and hence hypercholeresis, are particularly sensitive to the inhibitory effect of protoporphyrin IX.

scholarly journals Sodium Taurocholate Modifies the Bile Acid-Independent Fraction of Canalicular Bile Flow in the Rhesus Monkey

1979 ◽  
Vol 64 (1) ◽  
pp. 312-320 ◽  
Author(s):  
Alfred L. Baker ◽  
R. A. B. Wood ◽  
A. R. Moossa ◽  
James L. Boyer
Keyword(s):  
Bile Acid ◽  
Rhesus Monkey ◽  
Bile Flow ◽  
Sodium Taurocholate ◽  
Canalicular Bile

Effect of insulin on canalicular bile formation

1976 ◽  
Vol 231 (1) ◽  
pp. 40-43 ◽  
Author(s):  
RS Jones
Keyword(s):  
Bile Duct ◽  
Common Bile Duct ◽  
Intravenous Infusion ◽  
Bile Flow ◽  
Sodium Taurocholate ◽  
Duodenal Fistula ◽  
Bile Formation ◽  
Biliary Clearance ◽  
The Common ◽  
Bicarbonate Output

Mongrel dogs were prepared by cholecystectomy, ligation of the lesser pancreatic duct, and insertion of gastric and duodenal cannulas. The common bile duct was cannulated through the duodenal fistula. After bile flow had been stabilized by intravenous infusion of sodium taurocholate the dogs were given an intravenous injection of insulin or 0.9% NaCl (control). Insulin caused marked increases in bile flow, chloride output, and biliary clearance of erythritol and small increases in bicarbonate output and bile salt output. The increased erythritol clearance indicates that canalicular secretion contributes to insulin choleresis in dogs.

Intracellular chloride activity in intact rat liver: relationship to membrane potential and bile flow

1987 ◽  
Vol 252 (5) ◽  
pp. G699-G706
Author(s):  
J. G. Fitz ◽  
B. F. Scharschmidt
Keyword(s):  
Membrane Potential ◽  
Bile Flow ◽  
Chloride Transport ◽  
Basolateral Membrane ◽  
Bile Formation ◽  
Intracellular Chloride ◽  
Canalicular Bile ◽  
Intracellular Chloride Activity ◽  
Chloride Activity

Active chloride transport has been described in a variety of epithelia, and intracellular chloride activity (aiCl) in these tissues is generally elevated twofold or more above the level predicted for passive diffusion. To determine whether active chloride transport might contribute to canalicular bile formation, we have used conventional and Cl- -selective microelectrodes to measure aiCl of rat hepatocytes in vivo under a variety of conditions. Under basal conditions, the membrane potential difference averaged -33.2 +/- 3.5 mV (means +/- SD) in 29 animals, and the ratio (R) of observed aiCl (24.8 mM) to that expected for passive distribution at this membrane potential (22.6 mM) was 1.10 +/- 0.08, a value slightly but significantly greater than that predicted for passive distribution. Infusion of alanine (45-mumol bolus, 10.8-mumol/min infusion) in 5 animals hyperpolarized the membrane potential to -43.6 +/- 4.0 mV over 10-15 min and resulted in a significant fall in aiCl to 15.1 +/- 4.8 mM but with no change in R. Infusion of theophylline (577 nmol/min), taurocholate (3-mumol bolus, 810-nmol/min infusion), and ursodeoxycholic acid (4-mumol bolus, 2.13-mumol/min infusion) into 5 animals each increased bile flow by 6.1, 34.1, and 96.8%, respectively, compared with saline-infused controls but did not alter membrane potential or chloride distribution. These observations indicate that aiCl is close to the level predicted for passive distribution under basal conditions, after hyperpolarization of the membrane potential by alanine, and after stimulation of bile flow by a variety of choleretics. By analogy with Cl- -secreting epithelia, it appears unlikely that active chloride transport across the basolateral membrane contributes significantly to canalicular bile formation by the hepatocyte.

History of hepatic bile formation: old problems, new approaches

2014 ◽  
Vol 38 (4) ◽  
pp. 279-285 ◽  
Author(s):  
Norman B. Javitt
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Water Flow ◽  
Bile Flow ◽  
Water Movement ◽  
Sodium Taurocholate ◽  
Biliary System ◽  
Hepatic Bile ◽  
Bile Formation ◽  
Osmotic Effect

Studies of hepatic bile formation reported in 1958 established that it was an osmotically generated water flow. Intravenous infusion of sodium taurocholate established a high correlation between hepatic bile flow and bile acid excretion. Secretin, a hormone that stimulates bicarbonate secretion, was also found to increase hepatic bile flow. The sources of the water entering the biliary system with these two stimuli were differentiated by the use of mannitol. An increase in its excretion parallels the increase in bile flow in response to bile acids but not secretin, which led to a quantitative distinction between canalicular and ductular water flow. The finding of aquaglyceroporin-9 in the basolateral surface of the hepatocyte accounted for the rapid entry of mannitol into hepatocytes and its exclusion from water movement in the ductules where aquaporin-1 is present. Electron microscopy demonstrated that bile acids generate the formation of vesicles that contain lecithin and cholesterol after their receptor-mediated canalicular transport. Biophysical studies established that the osmotic effect of bile acids varies with their concentration and also with the proportion of mono-, di-, and trihydroxy bile acids and provides a basis for understanding their physiological effects. Because of the varying osmotic effect of bile acids, it is difficult to quantify bile acid independent flow generated by other solutes, such as glutathione, which enters the biliary system. Monohydroxy bile acids, by markedly increasing aggregation number, severely reduce water flow. Developing biomarkers for the noninvasive assessment of normal hepatic bile flow remains an elusive goal that merits further study.

scholarly journals A Single Adaptive Mutation in Sodium Taurocholate Cotransporting Polypeptide Induced by Hepadnaviruses Determines Virus Species Specificity

2018 ◽  
Vol 93 (5) ◽  
Author(s):  
Junko S. Takeuchi ◽  
Kento Fukano ◽  
Masashi Iwamoto ◽  
Senko Tsukuda ◽  
Ryosuke Suzuki ◽  
...  
Keyword(s):  
Amino Acid ◽  
Virus Infection ◽  
Positive Selection ◽  
Sodium Taurocholate ◽  
Arms Race ◽  
Adaptive Mutation ◽  
Molecular Evidence ◽  
Adaptive Mutations ◽  
Wide Range ◽  
Coevolutionary Arms Race

ABSTRACTHepatitis B virus (HBV) and its hepadnavirus relatives infect a wide range of vertebrates, from fish to human. Hepadnaviruses and their hosts have a long history of acquiring adaptive mutations. However, there are no reports providing direct molecular evidence for such a coevolutionary “arms race” between hepadnaviruses and their hosts. Here, we present evidence suggesting that the adaptive evolution of the sodium taurocholate cotransporting polypeptide (NTCP), an HBV receptor, has been influenced by virus infection. Evolutionary analysis of the NTCP-encoding genes from 20 mammals showed that most NTCP residues are highly conserved among species, exhibiting evolution under negative selection (dN/dSratio [ratio of nonsynonymous to synonymous evolutionary changes] of <1); this observation implies that the evolution of NTCP is restricted by maintaining its original protein function. However, 0.7% of NTCP amino acid residues exhibit rapid evolution under positive selection (dN/dSratio of >1). Notably, a substitution at amino acid (aa) 158, a positively selected residue, converting the human NTCP to a monkey-type sequence abrogated the capacity to support HBV infection; conversely, a substitution at this residue converting the monkey Ntcp to the human sequence was sufficient to confer HBV susceptibility. Together, these observations suggested a close association of the aa 158 positive selection with the pressure by virus infection. Moreover, the aa 158 sequence determined attachment of the HBV envelope protein to the host cell, demonstrating the mechanism whereby HBV infection would create positive selection at this NTCP residue. In summary, we provide the first evidence in agreement with the function of hepadnavirus as a driver for inducing adaptive mutation in host receptor.IMPORTANCEHBV and its hepadnavirus relatives infect a wide range of vertebrates, with a long infectious history (hundreds of millions of years). Such a long history generally allows adaptive mutations in hosts to escape from infection while simultaneously allowing adaptive mutations in viruses to overcome host barriers. However, there is no published molecular evidence for such a coevolutionary arms race between hepadnaviruses and hosts. In the present study, we performed coevolutionary phylogenetic analysis between hepadnaviruses and the sodium taurocholate cotransporting polypeptide (NTCP), an HBV receptor, combined with virological experimental assays for investigating the biological significance of NTCP sequence variation. Our data provide the first molecular evidence supporting that HBV-related hepadnaviruses drive adaptive evolution in the NTCP sequence, including a mechanistic explanation of how NTCP mutations determine host viral susceptibility. Our novel insights enhance our understanding of how hepadnaviruses evolved with their hosts, permitting the acquisition of strong species specificity.

scholarly journals Some biological indicators relevant for the management of cholestasis in children

2015 ◽  
Vol 67 (4) ◽  
pp. 1421-1424
Author(s):  
Evelina Moraru ◽  
Ana Drochioi ◽  
Paula Popovici ◽  
Carmen Anton ◽  
Laura Bozomitu ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Bile Flow ◽  
Serum Bilirubin ◽  
Biological Indicators ◽  
Aspartate Transaminase ◽  
Biological Parameters ◽  
Gamma Glutamyl Transpeptidase ◽  
Bile Formation ◽  
Diagnostic Protocol ◽  
Glutamyl Transpeptidase

Cholestasis is a multifactorial disorder with various biological, infectious, toxic, genetic and metabolic manifestations, its principal feature presented as reduced bile flow or abnormalities in bile formation. It has lately been accepted that some specific biological markers would shorten the period needed to establish a positive diagnosis, as currently it is necessary to navigate through a complex diagnostic protocol for this disorder. The purpose of this study was to establish some biological parameters and biomarkers useful for cholestasis management in children. Two hundred thirty-two children with cholestasis were selected, during a six-year study. The biological indicators followed were serum bilirubin, gamma-glutamyl transpeptidase, aspartate transaminase, alkaline phosphatase, lactate dehydrogenase, serum cholesterol and triglycerides. Our data showed that certain biological parameters are more often involved in the various forms of cholestasis, and the conclusions of this study could be useful in the early detection of cholestasis and appropriate disease management.

Differential effect of taurocholic acid on hepatic arterial resistance vessels and bile flow

1983 ◽  
Vol 244 (4) ◽  
pp. G366-G369 ◽  
Author(s):  
W. W. Lautt ◽  
T. R. Daniels
Keyword(s):  
Hepatic Artery ◽  
Bile Flow ◽  
Time Course ◽  
Parenchymal Cell ◽  
Taurocholic Acid ◽  
Metabolic Effects ◽  
Vascular Effects ◽  
Bile Formation ◽  
Liver Parenchymal Cell ◽  
Vascular Responses

The "hepatic arterial buffer response" hypothesis states that the hepatic artery is not controlled by liver parenchymal cell metabolic activity. Bile salts stimulate liver metabolism (elevate bile formation) and dilate the hepatic artery. The present data show that the vascular and metabolic effects in cats anesthetized with pentobarbital sodium are independent. Low doses of taurocholate (1 microM . min-1 . kg-1) produce metabolic but not vascular responses. At higher doses both the hepatic artery and superior mesenteric artery dilate with equal sensitivity. Taurocholate into the portal vein produced elevated bile flow and hepatic arterial dilation; infusion via the hepatic artery resulted in equal metabolic responses but much greater vascular effects. In addition, the time course of onset and termination of the metabolic and vascular responses supports the conclusion that the effects of taurocholic acid on hepatic bile flow and hepatic arterial flow are independent actions. This adds further support for the hepatic arterial buffer response being controlled by factors other than local hepatic metabolic demands.

Canalicular bile production in dogs

1968 ◽  
Vol 214 (4) ◽  
pp. 866-874 ◽  
Author(s):  
HO Wheeler ◽  
ED Ross ◽  
SE Bradley
Keyword(s):  
Canalicular Bile ◽  
Bile Production
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