This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Grau, M. Articles by Ramírez, I. Search for Related Content PubMed PubMed Citation Articles by Grau, M. Articles by Ramírez, I.

Interaction between Adrenaline and Epidermal Growth Factor in the Control of Liver Glycogenolysis in Mouse¹

Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain

Address all correspondence and requests for reprints to: Dr. Ignasi Ramírez, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Avda Diagonal 645, 08071-Barcelona, Spain. E-mail: sunyer{at}porthos.bio.ub.es

Epidermal growth factor (EGF) stimulates glycogenolysis in mouse liver, but the effect requires concentrations that are only achieved in plasma upon adrenergic stimulation of EGF release from submandibular salivary glands. Thus, we studied the interaction between adrenaline and EGF in liver glycogen metabolism, both in whole animals and in isolated hepatocytes. Adrenaline administered to anesthetized mice stimulated both the endocrine secretion of EGF from submandibular salivary glands and the degradation of glycogen in the liver. In sialoadenalectomized mice, adrenaline administration did not increase plasma EGF concentration. In these animals, the glycogenolytic response to adrenaline was enhanced. The sensitivity of hepatocytes to adrenaline was similar in cells from sialoadenalectomized and sham-operated mice. EGF, added to isolated hepatocytes, reduced the glycogenolytic effect of adrenaline (the maximal effect but not the ED₅₀). Adrenaline stimulated glycogen degradation through both an ₁-adrenergic mediated Ca²⁺ increase and a ß-adrenergic-mediated cAMP increase. EGF did not interfere with the rise of cytosolic Ca²⁺ but decreased the cAMP signal. EGF did not decrease the glycogenolytic effect of phenylephrine or VP (which increased cytosolic Ca²⁺ but not cAMP), but EGF decreased both the glycogenolytic effect and the cAMP signal generated by glucagon or forskolin. EGF did not interfere with the glycogenolytic effect of CPT-cAMP or bt₂-cAMP. The effect of EGF on cAMP was blocked by 3-isobutyl-1-methylxanthine. These results demonstrate that the effect of EGF on the glycogenolytic action of adrenaline involves interference with the generation of the cAMP signal. We suggest that EGF induces such an effect through the activation of a phosphodiesterase.

This article has been cited by other articles:

				O. Sanchez, M. Viladrich, I. Ramirez, and M. Soley Liver injury after an aggressive encounter in male mice Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2007; 293(5): R1908 - R1916. [Abstract] [Full Text] [PDF]

				L. Erraji-Benchekroun, D. Couton, C. Postic, I. Borde, J. Gaston, J.-G. Guillet, and C. Andre Overexpression of {beta}2-adrenergic receptors in mouse liver alters the expression of gluconeogenic and glycolytic enzymes Am J Physiol Endocrinol Metab, April 1, 2005; 288(4): E715 - E722. [Abstract] [Full Text] [PDF]

				M. Pareja, O. Sanchez, J. Lorita, M. Soley, and I. Ramirez Activated epidermal growth factor receptor (ErbB1) protects the heart against stress-induced injury in mice Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2003; 285(2): R455 - R462. [Abstract] [Full Text] [PDF]

				J. Lorita, N. Escalona, S. Faraudo, M. Soley, and I. Ramirez Effects of epidermal growth factor on epinephrine-stimulated heart function in rodents Am J Physiol Heart Circ Physiol, November 1, 2002; 283(5): H1887 - H1895. [Abstract] [Full Text] [PDF]