Hepatocyte bile secretion: Current views and controversies

Erlinger, S

doi:10.1002/hep.1840010413

Cited by 82 publications

(25 citation statements)

References 59 publications

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“…All solutions for intravenous infusion were prepared in Krebs-Henseleit bicarbonate solution, and fluid infusion rates were established using as a reference index the rate of bile flow and the value of the arterial hematocrit determined every 10 min. The hematocrit remained constant (42-46% in controls and 35-39% in BO rats) when the total rate of fluid infusion exceeded that of bile flow by at least 2 Cytochemistry and immunocytochemistry techniques. Smears of hepatocytes and nonparenchymal liver cells fixed in glutaraldehyde were used for cytochemical expression of glucose-6-phosphatase (G-6-P) as described by Wachstein and Meisel (16).…”

Section: Methodsmentioning

confidence: 95%

“…Current concepts indicate that bile is formed primarily at the bile canaliculus where osmotic gradients, generated by the biliary translocation of bile acids and/or other unidentified molecules, allow net movement of water from plasma into the canalicular lumen (1,2). Before reaching the duodenum or the gallbladder, however, canalicular bile is thought to be signifi-cantly modified while flowing through the collecting bile ductules and ducts.…”

Section: Introductionmentioning

confidence: 99%

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Biliary physiology in rats with bile ductular cell hyperplasia. Evidence for a secretory function of proliferated bile ductules.

Lenzi²,

et al. 1988

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To establish the role of the biliary epithelium in bile formation, we studied several aspects of biliary physiology in control rats and in rats with ductular cell hyperplasia induced by a 14-d extrahepatic biliary obstruction. Under steady-state conditions, spontaneous bile flow was far greater in obstructed rats (266.6±51.9 Mli/min per kg) than in controls (85.6±10.6 d1/ min per kg), while excretion of 3-hydroxy bile acids was the same in the two groups. Infusion of 10 clinical units (CU)/kg per h secretin produced a minimal choleretic effect in controls (+3.8±1.9 ,l/min per kg) but a massive increase in bile flow in the obstructed animals (+127.8±34.9 ,l/min per kg). Secretin choleresis was associated with an increase in bicarbonate biliary concentration and with a decline in 1'4C]mannitol bile-toplasma ratio, although solute biliary clearance significantly increased. Conversely, administration of taurocholate (5 ,umol/min per kg) produced the same biliary effects in control rats and in rats with proliferated biliary ductules. In the obstructed animals, the biliary tree volume measured during taurocholate choleresis (67.4±15.8 .I/g liver) was significantly greater than that determined during the increase in bile flow induced by secretin (39.5±10.4 ,l/g liver). These studies indicate that, in the rat, the proliferated bile ductules/ducts spontaneously secrete bile and are the site of secretin choleresis. Furthermore, because the proliferated cells expressed phenotypic traits of bile ductular cells, our results suggest that whereas under normal conditions the biliary ductules/ducts in the rat seem to contribute little to bile formation, secretion of water and electrolytes is a property of biliary epithelial cells.

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Section: Methodsmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Biliary physiology in rats with bile ductular cell hyperplasia. Evidence for a secretory function of proliferated bile ductules.

Lenzi²,

et al. 1988

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“…Secondary active transport processes energized by the transmembrane electrochemical sodium gradient attributable to Na,K-ATPase are currently believed to play a major role in absorption or secretion by a variety of epithelial tissues (3). Although Na,KATPase is also postulated to be important in bile formation (4)(5)(6), the precise role of this enzyme in bile acid-dependent (BADF)l and bile acid-independent (BAIF) bile formation remains poorly understood.…”

mentioning

confidence: 99%

“…Sodium transport and Na,K-ATPase also have generally been assumed to play a central role in bile acidindependent bile formation (4)(5)(6). Circumstantial evidence in support of this hypothesis includes the observations that (a) output of sodium, which accounts for a greater proportion of bile osmolality than any other solute (14,15), is linearly related to BAIF (16), (b) BAIF and hepatic Na,K-ATPase activity change in parallel following administration of certain agents (17)(18)(19)(20)(21)(22)(23), and (c) inhibitors of Na,K-ATPase diminish bile flow (24,25).…”

mentioning

confidence: 99%

Effects of ion substitution on bile acid-dependent and -independent bile formation by rat liver.

Dyke¹,

Stephens

Scharschmidt

1982

J. Clin. Invest.

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A B S T R A C T To characterize the transport mechanisms responsible for formation of canalicular bile, we have examined the effects of ion substitution on bile acid-dependent and bile acid-independent bile formation by the isolated perfused rat liver. Complete replacement of perfusate sodium with choline and lithium abolished taurocholate-induced choleresis and reduced biliary taurocholate output by >70%. Partial replacement of perfusate sodium (25 of 128 mM) by choline reduced bile acid-independent bile formation by 30% and replacement of the remaining sodium (103 mM) by choline reduced bile acid-independent bile formation by an additional 64%. In contrast, replacement of the remaining sodium (103 mM) by lithium reduced bile acid-independent bile formation by only an additional 20%, while complete replacement of sodium (128 mM) by lithium reduced bile formation by only 17%, and lithium replaced sodium as the predominant biliary cation. Replacement of perfusate bicarbonate by Tricine, a zwitterionic amino acid buffer, decreased bile acid-independent bile formation by >50% and decreased biliary bicarbonate output by -60%, regardless of the accompanying cation. In separate experiments, replacement of sodium by lithium essentially abolished Na,K-ATPase activity measured either as ouabain-suppressible ATP hydrolysis in rat liver or kidney homogenates, or as ouabain-suppressible 86Rb uptake by cultured rat hepatocytes.These studies indicate that bile acid(taurocholate)-dependent bile formation by rat liver exhibits a specific requirement for sodium, a finding probably attribPortions of this work were presented at the 82nd Annual

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“…However, the mechanisms operative in the transcytoplasmic transport and in the secretion of bile salts are not understood. The exitmechanism for bile salts may either be a carrier-mediated [7-91 or a vesicular process [58,59]. Assuming a carriermediated secretion process, it would be of interest to know if the same type of carrier is involved as for the uptake.…”

Section: Photouffinity Labelling Qf Plusma Membrane Subfructions Prdomentioning

confidence: 99%

Bile‐Salt‐Binding Polypeptides in Plasma Membranes of Hepatocytes Revealed by Photoaffinity Labelling

Kramer

Bickel

Buscher

et al. 1982

European Journal of Biochemistry

129

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1. Photoaffinity labelling of a subfraction of plasma membranes of rat liver, enriched with sinusoidal surfaces, with the sodium salts of (3~-azido-7a,l2r~-dihydroxy-5~-cholan-24-oyl)-2-amino[2-~H(N)]ethanesulfoni acid, (7,7-azo-3r~,12a-dihydroxy-5~-cholan-24-oyl)-2-amino[2-~H(N)]ethanesulfonic acid and ( 1 I~-azido-12-oxo3r,7a-dihydroxy-5~-cholan-24-oyl)-2-amino[2-3H(N)]ethanesulfonic acid resulted with each derivative in a clear covalent incorporation of radioactivity into polypeptides with the apparent molecular weights of 67 000, 52 000, 48000,43000 and about 20000.2. Photoaffinity labelling of a membrane subfraction predominantly composed of bile canalicular membranes by the photolabile derivatives of the conjugated bile salts also showed covalent incorporation of radioactivity into polypeptides of the same apparent molecular weights as with the subfraction enriched with the sinusoidal membranes.3. The extent of photoaffinity labelling of the different membrane polypeptides is dependent upon the photolabile bile-salt derivative used. However, with each of the photolabile derivatives the relative ratio of the labelling of the different membrane polypeptides was similar for both membrane subfractions. Provided that the uptake as well as the secretion of bile salts by hepatocytes are carrier-mediated processes, this suggests the participation of the same polypeptides in both processes.In the course of enterohepatic circulation, bile salts are taken up by the hepatocyte from portal blood and secreted into the bile. This functional polarity becomes morphologically apparent in a regional specialization of the surface membrane in areas for uptake and for secretion. Both the uptake by the sinusoidal membrane and the secretion by the bile canalicular membrane seem to be carrier-mediated transport processes [I -91, the secretion being the rate-limiting step in the over-all transport from blood to bile [7,8]. Under physiological conditions conjugated and unconjugated bile salts cross the sinusoidal cell membrane. Based on kinetic measurements, more than one carrier for the uptake of bile salts by hepatocytes has been postulated [lo, 111. These different carriers are assumed to be partly specific for the conjugated derivatives and to be partly shared by conjugated and unconjugated bile salts [I I].Most investigations so far have been concerned with the characterization of the kinetics of uptake and secretion processes for bile salts, and only a few studies have been perAbbreviation. Hepes, 4-(2-hydroxyethyI)-l-piperazineethanesulfonic acid.Enzyrnc~.

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Hepatocyte bile secretion: Current views and controversies

Cited by 82 publications

References 59 publications

Biliary physiology in rats with bile ductular cell hyperplasia. Evidence for a secretory function of proliferated bile ductules.

Biliary physiology in rats with bile ductular cell hyperplasia. Evidence for a secretory function of proliferated bile ductules.

Effects of ion substitution on bile acid-dependent and -independent bile formation by rat liver.

Bile‐Salt‐Binding Polypeptides in Plasma Membranes of Hepatocytes Revealed by Photoaffinity Labelling

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