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URN: urn:nbn:de:kobv:517-opus-45792
URL: http://opus.kobv.de/ubp/volltexte/2010/4579/


Püschel, Gerhard ; Christ, Bruno

Inhibition by PGE₂ of glucagon-induced increase in phosphoenolpyruvate carboxykinase mRNA and acceleration of mRNA degradation in cultured rat hepatocytes

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Kurzfassung in Englisch

In cultured rat hepatocytes the key gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PCK) is known to be induced by glucagon via an elevation of cAMP. Prostaglandin E₂ has been shown to antagonize the glucagon-activated cAMP formation, glycogen phosphorylase activity and glucose output in hepatocytes. It was the purpose of the current investigation to study the potential of PGE₂ to inhibit the glucagon-induced expression of PCK on the level of mRNA and enzyme activity. PCK mRNA and enzyme activity were increased by 0.1 nM glucagon to a maximum after 2 h and 4 h, respectively. This increase was completely inhibited if 10 μM PGE2 was added concomitantly with glucagon. This inhibition by PGE₂ of glucagon-induced PCK activity was abolished by pertussis toxin treatment. When added at the maximum of PCK mRNA at 2 h, PGE₂ accelerated the decay of mRNA and reduced enzyme activity. This effect was not reversed by pertussis toxin treatment. Since in liver PGE₂ is derived from Kupffer cells, which play a key role in the local inflammatory response, the present data imply that during inflammation PGE₂ may reduce the hepatic gluconeogenic capacity via a Gᵢ-linked signal chain.

Freie Schlagwörter (Englisch): Prostaglandin E₂ , Glucagon , Phosphoenolpyruvate carboxykinase , Inflammation , mRNA degradation
Institut: Institut für Ernährungswissenschaft
DDC-Sachgruppe: Biowissenschaften, Biologie
Dokumentart: c Postprint
Schriftenreihe: Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe, ISSN 1866-8372
Bandnummer: paper 045
Quelle: FEBS Letters 351 (1994), 3, p. 353-356, DOI 10.1016/0014-5793(94)00877-9, ISSN 0014-5793
Sprache: Englisch
Erstellungsjahr: 1994
Publikationsdatum: 03.08.2010
Bemerkung:
first published in:
FEBS Letters - 351 (1994), 3, p. 353-356
ISSN: 0014-5793
doi: 10.1016/0014-5793(94)00877-9
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