The induction of glycogenolysis in the perfused liver by platelet activating factor is mediated by prostaglandin D2 from Kupffer cells |
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Authors: | J Kuiper Y B De Rijke F J Zijlstra M P Van Waas T J Van Berkel |
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Affiliation: | Division of Biopharmaceutics, Sylvius Laboratories, University of Leiden, The Netherlands. |
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Abstract: | Induction of glycogenolysis in the perfused liver by platelet activating factor (PAF) was blocked by the cyclooxygenase inhibitor indomethacin. 3H-labeled PAF was shown to interact in the perfused liver primarily with Kupffer cells. The addition of PAF to Kupffer cells resulted in a dose-dependent stimulation of prostaglandin D2 (PGD2) production, which was identified as the main eicosanoid formed after PAF stimulation of the Kupffer cells. PGD2 was able to induce a dose-dependent stimulation of glycogenolysis both in the perfused liver and in isolated parenchymal cells. The time-dependency of the PGD2 production and the glucose output by the perfused liver is consistent with a primary interaction of PAF with the Kupffer cells, followed by PGD2 formation, which subsequently stimulates glucose production in parenchymal cells. |
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