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

doi:10.1530/JOE-15-0463

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 journal › Article › peer-review

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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	https://doi.org/10.1530/JOE-15-0463
Publication status	Published (in print/issue) - 1 Jun 2016

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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1530/JOE-15-0463

JOE-15-0463Author Accepted Manuscript, 2.44 MB

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title = "Glucagon receptor antagonist and GIP agonist combination for diet induced obese mice.",

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",

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author = "L McShane and Nigel Irwin and D O'Flynn and Z Franklin and C Hewage and Finbarr O'Harte",

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T1 - Glucagon receptor antagonist and GIP agonist combination for diet induced obese mice.

AU - McShane, L

AU - Irwin, Nigel

AU - O'Flynn, D

AU - Franklin, Z

AU - Hewage, C

AU - O'Harte, Finbarr

PY - 2016/6/1

Y1 - 2016/6/1

N2 - 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

AB - 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

KW - glucagon

KW - glucose-dependent insulinotropic polypeptide (GIP)

KW - glucose 25 homeostasis

KW - insulin secretion

KW - insulin sensitivity

KW - glucagon receptor antagonist

KW - GIP receptor agonist

KW - diet nduced obese diabetic mice

U2 - 10.1530/JOE-15-0463

DO - 10.1530/JOE-15-0463

M3 - Article

SN - 1479-6805

VL - 229

SP - 319

EP - 330

JO - Journal of Endrocrinology

JF - Journal of Endrocrinology

ER -

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

Abstract

Keywords

UN SDGs

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