Endotoxin stimulates glycogenolysis in the liver by means of intercellular communication.

Casteleijn, Eric; Kuiper, Johan; Rooij, H. C. J. Van; Kamps, Jan A. A. M.; Koster, J.F.; Berkel, Theo J.C. Van

doi:10.1016/s0021-9258(18)68587-4

Cited by 110 publications

(1 citation statement)

References 16 publications

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“…Sie werden von Nichtparenchymzellen als Antwort auf eine große Anzahl entzündlicher Stimuli wie LPS (Kuiper et al 1988), Zymosan (Dieter et al 1989), Anaphylatoxine (Hespeling et al 1995;Püschel et al 1993) und proinflammatorische Cytokine wie TNFα freigesetzt. Die freigesetzten Prostanoide modulieren Funktionen von Hepatocyten in parakriner Weise: Sie beeinflussen die glucogene Aktivität der Hepatocyten durch die Regulation von Enzymaktivitäten (Püschel et al 1993a;Casteleijn et al 1988;Brass und Garrity 1985;Bronstad und Christoffersen 1981), durch die Kontrolle der Expressionsspiegel von glucogenen Schlüsselenzymen (Püschel und Christ 1994) und indirekt auch durch eine Modulation des sinusoidalen Blutflusses (Schieferdecker et al 1999).…”

Section: Prostanoid-vermittelte Interzelluläre Kommunikationunclassified

Einschränkung hepatischer Abwehrreaktionen während einer Entzündung durch Prostaglandin E2 über Gs-Protein-gekoppelte Prostaglandin E2-Rezeptoren

Fennekohl¹

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Section: Prostanoid-vermittelte Interzelluläre Kommunikationunclassified

Einschränkung hepatischer Abwehrreaktionen während einer Entzündung durch Prostaglandin E2 über Gs-Protein-gekoppelte Prostaglandin E2-Rezeptoren

Fennekohl¹

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Zymosan-induced changes in glucose release and fatty acid oxidation in the perfused rat liver

Derbocio¹,

Bracht²,

Constantin³

et al. 2000

J. Biochem. Mol. Toxicol.

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The aim of the present study was to investigate the actions of zymosan on glucose release and fatty acid oxidation in perfused rat livers and to determine if Kupffer cells and Ca2+ ions are implicated in these actions. Zymosan caused stimulation of glycogenolysis in livers from fed rats. In livers from fasted rats zymosan caused gradual inhibition of glucose production and oxygen consumption from lactate plus pyruvate. Ketogenesis, oxygen consumption, and [14C‐]‐CO2 production were inhibited by zymosan when the [1‐14C]‐palmitate was supplied exogenously. However, ketogenesis and oxygen consumption from endogenous sources were not inhibited. An interference with substrate‐uptake by the liver may be the cause of the changes in gluconeogenesis and oxidation of fatty acids from exogenous sources. The pretreatment of the rats with gadolinium chloride and the removal of Ca2+ ions did not suppress the effects of zymosan on glucose release, a finding that argues against the participation of Kupffer cells or Ca2+ ions in the liver responses. The hepatic metabolic changes caused by zymosan could play a role in the systemic metabolic alterations reported to occur after in vivo zymosan administration. © 2000 John Wiley & Sons, Inc. J Biochem Toxicol 14:252–261, 2000

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Increased bioavailability of enzymes of eicosanoid synthesis in hepatic and extrahepatic tissues after portacaval shunting

et al. 1989

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Metabolites of arachidonic acid have been attributed to severe circulatory, metabolic and hormonal alterations in patients with chronic liver disease. In order to study changes of the tissue-specific availability of enzymes of eicosanoid synthesis, we used portacaval-shunted rats, as this model exhibits many clinical and biochemical similarities to patients suffering from cirrhosis of the liver. Microsomal mass and maximal velocity of prostaglandin H synthase, the initial enzyme of prostaglandin synthesis, were markedly and permanently increased after shunting in both hepatic and extrahepatic tissues as compared to those of sham-operated rats. Maximal velocity of thromboxane synthase and prostacyclin synthase, two more peripheral enzymes of the arachidonic acid cascade, were tissue-specifically enhanced, whereas the apparent affinities (Km) remained unchanged. Determination of 5-lipoxygenase activity in tissue preparations disclosed a preferential increase in the liver, lung and renal cortex after portacaval shunting. Furthermore, exposure to endotoxin closely mimicked the shunting-induced changes. These results suggest that after portacaval shunting and possibly in patients with advanced liver disease, profound abnormalities at the level of local enzyme expression might play a pathophysiologically important role in the control of eicosanoid synthesis.

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Endotoxin stimulates glycogenolysis in the liver by means of intercellular communication.

Cited by 110 publications

References 16 publications

Einschränkung hepatischer Abwehrreaktionen während einer Entzündung durch Prostaglandin E2 über Gs-Protein-gekoppelte Prostaglandin E2-Rezeptoren

Einschränkung hepatischer Abwehrreaktionen während einer Entzündung durch Prostaglandin E2 über Gs-Protein-gekoppelte Prostaglandin E2-Rezeptoren

Zymosan-induced changes in glucose release and fatty acid oxidation in the perfused rat liver

Increased bioavailability of enzymes of eicosanoid synthesis in hepatic and extrahepatic tissues after portacaval shunting

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