Molecular and cellular aspects of the glucagon receptor: Role in diabetes and metabolism

R. Burcelin, E. B. Katz, M. J. Charron

Research output: Contribution to journalReview article

79 Scopus citations

Abstract

The role of glucagon in eliciting hyperglycaemia has been studied extensively for more than 20 years. However, little has been learned about the specific targeted tissues and intracellular effects of glucagon since no specific causal interactions have been established between glucagon and the so called 'glucagon-binding site'. Indeed, glucagon and related hormones, such as glucagon-like peptide, glucoinsulinotropic hormone and vasoactive intestinal peptide acting through different receptors, have similar effects in hyperglycaemic syndromes. The recent cloning of the glucagon receptor (GR) encoding sequences has clarified many aspects of its structure as well as its integrated role in the cell and the entire body. The GR contains seven transmembrane domains and is characterised by a conserved G-protein binding site and a large amino-terminal domain containing the amino-acid residues mainly involved in ligand binding. The GR is expressed in liver, pancreatic beta cells, kidney, adipose tissues, heart, and vascular tissues, as well as in some region of brain, stomach, and adrenal glands. The precise role of the GR in most of these tissues is still unclear. However, with the cloning of the coding sequences, genetic manipulations of the GR should provide specific indications of the normal metabolic effects of the GR system on these tissues and how altered glucagon signalling might contribute to the development of diabetes.

Original languageEnglish (US)
Pages (from-to)373-396
Number of pages24
JournalDiabetes and Metabolism
Volume22
Issue number6
Publication statusPublished - Dec 1 1996

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Keywords

  • GTP-binding protein-coupled receptor
  • gene cloning liver
  • glucose production
  • seven transmembrane domain receptor

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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