Title: Modulation of maximal glycogenolysis in perfused rat liver by adenosine and ATP
Authors: Vanstapel, Florent ×
Waebens, Marleen
Van Hecke, Paul
Decanniere, C
Stalmans, Willy #
Issue Date: Sep-1991
Series Title: The Biochemical journal. vol:277 ( Pt 3) pages:597-602
Abstract: Rat livers perfused at constant flow via the portal vein with dibutyryl cyclic AMP produced glucose equivalents at a steady maximal rate (6 mumol/min per g of liver). Addition of adenosine (150 microM) caused a biphasic effect. (i) First, the glycogenolytic rate rose transiently, to a mean peak of 150% of control levels after 2 min. This glycogenolytic burst was reproduced by two P1-receptor agonists, but not by ATP, and was blocked by a P1-antagonist (8-phenyltheophylline), as well as by inhibitors of eicosanoid synthesis (indomethacin, ibuprofen or aspirin). It did not occur in phosphorylase-kinase-deficient livers. The adenosine-induced glycogenolytic burst coincided with moderate and transient changes in portal pressure (+6 cmH2O) and O2 consumption (-20%), but it could not be explained by an increase in cytosolic Pi, since the n.m.r. signal fell precipitously. (ii) Subsequently, the rate of glycogenolysis decreased to one-third of the preadenosine value, in spite of persistent maximal activation of phosphorylase. The decrease could be linked to the decline in cytosolic Pi: both changes were prevented by the adenosine kinase inhibitor 5-iodotubercidin, whereas they were not affected by ibuprofen or 8-phenyltheophylline, and were not reproduced by non-metabolized adenosine analogues. In comparison with adenosine, ATP caused a slower decrease of Pi and of glycogenolysis. The fate of the cytosolic Pi was unclear, especially with administered ATP, which did not increase the n.m.r.-detectable intracellular ATP.
ISSN: 0264-6021
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Radiology
Laboratory of Clinical Bacteriology and Mycology
Department of Cellular and Molecular Medicine - miscellaneous
Biomedical Quality Assurance Research Unit
× corresponding author
# (joint) last author

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