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URN: urn:nbn:de:kobv:517-opus-16697
URL: http://opus.kobv.de/ubp/volltexte/2008/1669/


Hespeling, Ursula ; Jungermann, Kurt ; Püschel, Gerhard P.

Feedback-inhibition of glucagon-stimulated glycogenolysis in hepatocyte/kupffer cell cocultures by glucagon-elicited prostaglandin production in kupffer cells

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Kurzfassung auf Englisch

Prostaglandins, released from Kupffer cells, have been shown to mediate the increase in hepatic glycogenolysis by various stimuli such as zymosan, endotoxin, immune complexes, and anaphylotoxin C3a involving prostaglandin (PG) receptors coupled to phospholipase C via a G(0) protein. PGs also decreased glucagon-stimulated glycogenolysis in hepatocytes by a different signal chain involving PGE(2) receptors coupled to adenylate cyclase via a G(i) protein (EP(3) receptors). The source of the prostaglandins for this latter glucagon-antagonistic action is so far unknown. This study provides evidence that Kupffer cells may be one source: in Kupffer cells, maintained in primary culture for 72 hours, glucagon (0.1 to 10 nmol/ L) increased PGE(2), PGF(2 alpha), and PGD(2) synthesis rapidly and transiently. Maximal prostaglandin concentrations were reached after 5 minutes. Glucagon (1 nmol/L) elevated the cyclic adenosine monophosphate (cAMP) and inositol triphosphate (InsP(3)) levels in Kupffer cells about fivefold and twofold, respectively. The increase in glyco gen phosphorylase activity elicited by 1 nmol/L glucagon was about twice as large in monocultures of hepatocytes than in cocultures of hepatocytes and Kupffer cells with the same hepatocyte density. Treatment of cocultures with 500 mu mol/L acetylsalicylic acid (ASA) to irreversibly inhibit cyclooxygenase (PGH-synthase) 30 minutes before addition of glucagon abolished this difference. These data support the hypothesis that PGs produced by Kupffer cells in response to glucagon might participate in a feedback loop inhibiting glucagon-stimulated glycogenolysis in hepatocytes.

Freie Schlagwörter (englisch): perfused-rat-liver , aggregated immunoglobulin-g , intercellular communication , adenylate-cyclase , arachidonic-acid , activation , glucose
Institut: Institut für Ernährungswissenschaft
DDC-Sachgruppe: Biowissenschaften, Biologie
Dokumentart: c Postprint
Schriftenreihe: Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe, ISSN 1866-8372
Band Nummer: paper 036
Quelle: Hepatoloy. - ISSN 0270-9139. - 22 (1995), 5, p. 1577 - 1583
Sprache: Englisch
Erstellungsjahr: 1995
Publikationsdatum: 10.03.2008
Bemerkung:
first published in:
Hepatology - 22 (1995), 5 p. 1577 - 1583
ISSN: 0270-9139
doi: 10.1002/hep.1840220534
Lizenz: Diese Nutzungsbedingung gilt nicht, wenn in den Metadaten eine modifizierende Lizenz genannt ist. Keine Nutzungslizenz vergeben - es gilt das deutsche Urheberrecht


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