Abstract
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 language | English |
|---|---|
| Pages (from-to) | 319-330 |
| Journal | Journal of Endrocrinology |
| Volume | 229 |
| Early online date | 20 Apr 2016 |
| DOIs | |
| Publication status | Published (in print/issue) - 1 Jun 2016 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- 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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