Glucagon receptor antagonist and GIP agonist combination for diet induced obese mice.

L McShane, Nigel Irwin, D O'Flynn, Z Franklin, C Hewage, Finbarr O'Harte

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)
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Ablation of glucagon receptor signalling represents a potential treatment option for type 2 diabetes (T2DM). Additionally, activation of glucose-dependent insulinotropic polypeptide (GIP) receptor signalling also holds therapeutic promise for T2DM. Therefore, the present study examined both independent and combined metabolic actions of desHis1Pro4Glu9(Lys12PAL)-glucagon (glucagon receptor antagonist) and D-Ala2GIP (GIP receptor agonist), in diet induced obese mice. Glucagon receptor binding has been linked to alpha-helical structure and desHis1Pro4Glu9(Lys12PAL)-glucagon displayed enhanced alpha-helical content compared to native glucagon. In clonal pancreatic BRIN-BD11 beta-cells, desHis1Pro4Glu9(Lys12PAL)-glucagon was devoid of any insulinotropic or cAMP generating actions, and did not impede D-Ala2GIP-mediated (p
Original languageEnglish
Pages (from-to)319-330
JournalJournal of Endrocrinology
Early online date20 Apr 2016
Publication statusPublished (in print/issue) - 1 Jun 2016


  • glucagon
  • glucose-dependent insulinotropic polypeptide (GIP)
  • glucose 25 homeostasis
  • insulin secretion
  • insulin sensitivity
  • glucagon receptor antagonist
  • GIP receptor agonist
  • diet nduced obese diabetic mice


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