Metabolic effects and cyclic AMP levels produced by glucagon, (1-Nα-trinitrophenylhistidine,12-homoarginine)glucagon and forskolin in isolated rat hepatocytes

Silvia Corvera, Judith Huerta-Bahena, John T. Pelton, Victor J. Hruby, Dev Trivedi, J. Adolfo García-Sáinz

Research output: Contribution to journalArticle

31 Scopus citations

Abstract

[1-Nα-Trinitrophenylhistidine,12-homoarginine]glucagon (THG) is a potent antagonist of the effects of glucagon on liver membrane adenylate cyclase. In isolated hepatocytes, this glucagon analogue was an extremely weak partial agonist for cAMP accumulation, and it blocked the stimulation of cAMP accumulation produced by glucagon. However, THG was a full agonist for the stimulation of glycogenolysis, gluconeogenesis and urea synthesis in rat hepatocytes, and did not antagonize the metabolic effects of glucagon under most of the conditions examined. Forskolin potentiated the stimulation of cAMP accumulation produced by glucagon or THG, but did not potentiate their metabolic actions. A much larger increase in cAMP levels seemed to be required for the stimulation of hepatocyte metabolism by forskolin than by glucagon or THG. This may suggest the existence of a functional compartmentation of cAMP in rat hepatocytes. The possible existence of compartments in cAMP-mediated hormone actions and the involvement of factors, besides cAMP, in mediating the effects of THG and glucagon is suggested.

Original languageEnglish (US)
Pages (from-to)434-441
Number of pages8
JournalBBA - Molecular Cell Research
Volume804
Issue number4
DOIs
StatePublished - Aug 17 1984

Keywords

  • (Rat hepatocyte)
  • Forskolin
  • Glucagon
  • Glucagon analog
  • cyclic AMP

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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