Dissection of compartments in rat hepatocytes involved in the intracellular trafficking of high‐density lipoprotein particles or their selectively internalized cholesteryl esters

Stefan Jäckle, Franz Rinninger, Thomas Lorenzen, Heiner Greten, Eberhard Windler – 1 March 1993 – The trafficking of apolipoprotein E–deficient highdensity lipoprotein particles and of their component cholesteryl esters in rat hepatocytes was studied. Human high‐density lipoprotein 3, labeled with two nondegradable, intracellularly trapped tracers in their apolipoprotein A–I and their cholesteryl esters, were injected into rats, and five subcellular hepatocytic fractions were isolated at various time intervals.

Effects of dietary cholesterol on bile formation and hepatic processing of chylomicron remnant cholesterol in the rat

Martin J. Smit, Folkert Kuipers, Roel J. Vonk, Arno M. Temmerman, Stefan Jäckle, Eberhard E. T. Windler – 1 March 1993 – We have studied the coupling between hepatic uptake of chylomicron remnant cholesteryl ester and biliary excretion of cholesterol and bile acids in rats, after feeding them a cholesterol‐free (control) or a high‐cholesterol diet (1% wt/wt) for 2 wk. We equipped rats with permanent catheters in the bile duct, duodenum and heart to allow experiments in unanesthetized, unrestrained animals.

Accumulation of organic anion in intracellular vesicles of cultured rat hepatocytes is mediated by the canalicular multispecific organic anion transporter

Ronald P. J. Oude Elferink, Conny T. M. Bakker, Han Roelofsen, Esther Middelkoop, Roelof Ottenhoff, Marc Heijn, Peter L. M. Jansen – 1 March 1993 – Transport of organic anions within hepatocytes and the possible involvement of intracellular vesicles were studied with fluorescence microscopy. For this purpose monochlorobimane, a nonfluorescent hydrophobic compound that readily permeates into cells and is conjugated with glutathione to form the fluorescent glutathione bimane, was used. In the isolated perfused livers of normal rats, glutathione bimane is rapidly secreted into bile.

Hemodynamic and humoral changes after liver transplantation in patients with cirrhosis

Miquel Navasa, Faust Feu, Joan Carles García‐Pagan, Wladimiro Jiménez, Josep Llach, Antoni Rimola, Jaume Bosch, Joan Rodés – 1 March 1993 – Splanchnic and systemic hemodynamics and plasma levels of aldosterone, glucagon and plasma renin were investigated in 12 patients with advanced cirrhosis before and 2 wk (14.6 ± 2.8 days) and 2 mo (60.8 ± 10.5 days) after orthotopic liver transplantation. Liver transplant was followed by significant (p < 0.01) changes in systemic hemodynamics at 2 wk, with a marked reduction in cardiac index (4.9 ± 0.8 vs.

Is vesicular exocytosis and membrane recycling a mechanism for secretin‐induced choleresis in bile duct epithelium?

Jorge J. Gumucio, Won Kyoo Cho, James L. Broder – 1 March 1993 – Intrahepatic bile duct epithelial cells, or cholangiocytes, contribute to bile secretion in response to hormones, including secretin. However, the mechanism by which secretin stimulates ductular bile flow is unknown. Since recent data in nonhepatic epithelia have suggested a role for exocytosis in fluid secretion, we tested the hypothesis that secretin stimulates exocytosis by isolated cholangiocytes.

Tauroursodeoxycholate and tauro‐β‐muricholate exert cytoprotection by reducing intrahepatocyte taurochenodeoxycholate content

Takayuki Ohiwa, Kenji Katagiri, Makoto Hoshino, Tomihiro Hayakawa, Tomio Nakai – 1 March 1993 – Cytoprotection by tauroursodeoxycholic acid and tauro‐β‐muricholic acid against taurochenodeoxycholic acid–induced toxicity was examined with reference to intracellular bile acid content in primary cultured rat hepatocytes.

Administration of hepatic stimulatory substance alone or with other liver growth factors does not ameliorate acetaminophen‐induced liver failure

Antonio Francavilla, Alessandro Azzarone, Guiseppe Carrieri, Umberto Cillo, David Van Thiel, Vladimir Subbottin, Thomas E. Starzl – 1 March 1993 – Sixty‐two beagle dogs were given three doses of acetaminophen over a period of 24 hr in a fulminant liver failure model that is 70% lethal in 72 hr. Treatment of the animals with hepatic stimulatory substance alone or in a mixture with insulin, transforming growth factor‐α and insulin‐like growth factor II had no effect on mortality.

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