Modulation of platelet activating factor-induced glycogenolysis in the perfused rat liver after administration of endotoxin in vivo.

Kimura K, Moriyama M, Nishisako M, Kannan Y, Shiota M, Sakurada K, Musashi M, Sugano T
J Biochem. 1998 123 (1): 142-9

PMID: 9504421 · DOI:10.1093/oxfordjournals.jbchem.a021901

The effect of endotoxin treatment in vivo on platelet activating factor (PAF)-induced glycogenolysis was studied in the perfused rat liver. The addition of PAF (20 nM) to the perfusate increased glucose production concomitant with suppression of oxygen consumption in control rats without endotoxin treatment. At 6 h after endotoxin administration, PAF caused severe suppression of oxygen consumption, but glucose production was greatly inhibited. At 24 h after endotoxin treatment, PAF caused less suppression of oxygen consumption than the control, and glucose production was partially restored. The metabolic responses in the control rat were abolished by the simultaneous presence of cyclooxygenase- and lipoxygenase-inhibitors. Combined use of leukotriene (LT) D4- and thromboxane (Tx) A2-receptor antagonists inhibited the metabolic responses in the rat given endotoxin 6 h before. The efflux of Tx B2 during PAF-infusion decreased 24 h after endotoxin treatment, and Tx A2 receptor antagonist, but not LT D4 receptor antagonist, prevented the suppression of oxygen consumption. These results suggest that different eicosanoids are involved in PAF-induced glycogenolysis in different stages of endotoxemia, and that LT D1 may also play a role in PAF-induced glycogenolysis.

MeSH Terms (21)

Animals Eicosanoids Endotoxemia Glycogen Leukotriene Antagonists Leukotriene D4 Lipopolysaccharides Liver Male Membrane Proteins Oxygen Consumption Perfusion Platelet Activating Factor Prostaglandin D2 Rats Rats, Sprague-Dawley Receptors, Immunologic Receptors, Leukotriene Receptors, Prostaglandin Receptors, Thromboxane Thromboxane A2

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