Glucose release as a response to glucagon in rat hepatocyte culture: involvement of NO signaling

Title:

Glucose release as a response to glucagon in rat hepatocyte culture: involvement of NO signaling

Creator:

Hassan Farghali, Hodis, J., Nikolína Kutinová-Canová, Petr Potměšil, Eva Kmoníčková, and Zdeněk Zídek

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:0fe91736-a85d-4c9c-94dd-083dcbe17f52
uuid:0fe91736-a85d-4c9c-94dd-083dcbe17f52
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, farmakologie, oxid dusnatý, glukagon, jaterní buňky, pharmacology, nitric oxide, glucagon, liver cells, glycogenolysis, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Glucagon and α-adrenergic-induced glycog enolysis 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 (NO2-) was assessed under the influence of glucagon, dibutyryl cyclic AMP (db-cAMP), forskolin, the nitric oxide synthase (NOS) inhibitors Nω-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine, and the NO donor S-nitroso-N-acetyl penicillamine (SNAP). Inducible NOS (iNOS) mRNA was examined by reverse transcription-polymerase chain reaction. Glycogenolysis was followed up by estimation of medium glucose levels. The amount of glucose and NO2- released by glycogen-rich hepatocytes was increased as a result of glucagon, db-cAMP, forskolin and SNAP treatments. iNOS gene expression was upregulated by glucagon. Glycogenolysis that occurs through glucagon receptor stimulation involves NO production downstream of transduction pathways through an isoform of NO synthase. The present and previous studies document possible involvement of NO signaling in glycogenolytic response to glucagon and adrenergic agonists in hepatocytes., H. Farghali, J. Hodis, N. Kutinová-Canová, P. Potměšil, E. Kmoníčková, Z. Zídek., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2008 Volume:57 | Number:4

Harvested from:

CDK

Metadata only:

false