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The induction of glycogenolysis in the perfused liver by platelet activating factor is mediated by prostaglandin D2 from Kupffer cells.

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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Kuiper J,De Rijke YB,Zijlstra FJ,Van Waas MP,Van Berkel TJ

doi

10.1016/s0006-291x(88)81014-3

subject

Has Abstract

pub_date

1988-12-30 00:00:00

pages

1288-95

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(88)81014-3

journal_volume

157

pub_type

杂志文章

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