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Glucose Release as a Response to Glucagon in Rat Hepatocyte Culture: Involvement of NO Signaling
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Physiological Research
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July 1, 2008
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Copyright informationCopyright Institute of Physiology 2008. Provided by ProQuest LLC. (Hide copyright information)
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Summary
Glucagon and α-adrenergic-induced glycogenolysis is realized via the agonist/adenylyl cyclase/cAMP/protein kinase signaling pathway or via the activation of phosphorylase kinase by the mobilized calcium that supports the inhibition of glycogen synthase, respectively. The role of nitric oxide (NO) in this process has not been extensively studied. The present work was directed to the question whether NO is produced during glucagon-induced glycogenolysis in rat hepatocyte in a similar way like α-adrenoceptor stimulation. Glycogen-rich hepatocyte cultures were used. NO production (NO^sub 2^^sup -^) was assessed under the influence of glucagon, dibutyryl cyclic AMP (db-cAMP), ...
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