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Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone secreted by endocrine K-cells in response to nutrient absorption. This study has utilised numerous well-characterised dipeptidyl peptidase IV-resistant GIP analogues to evaluate the glucagonotropic actions of GIP in Wistar rats and isolated rat islets. Intraperitoneal administration of GIP analogues (25 nmol/kg body weight) in combination with glucose had no effect on circulating glucagon concentrations compared to controls in Wistar rats. However, plasma glucose concentrations were significantly ( p &lt;0.05 to  p &lt;0.001) lowered by the GIP-receptor agonists,  N -AcGIP, GIP(Lys 37 )PAL and  N -AcGIP(Lys 37 )PAL. The GIP antagonist, (Pro 3 )GIP, caused a significant ( p &lt;0.05) reduction in glucagon levels following concurrent administration with saline in Wistar rats. In isolated rat islets native GIP induced a significant ( p &lt;0.01) enhancement of glucagon release at basal glucose concentrations, which was completely annulled by (Pro 3 )GIP. Furthermore, glucagon release in the presence of GLP-1, GIP(Lys 37 )PAL,  N -AcGIP(Lys 37 )PAL and (Pro 3 )GIP was significantly ( p &lt;0.05 to  p &lt;0.001) decreased compared to native GIP in isolated rat islets. These data indicate a modest effect of GIP on glucagon secretion from isolated rat islets, which was not observed  in vivo . However, the GIP agonists  N -AcGIP, GIP(Lys 37 )PAL and  N -AcGIP(Lys 37 )PAL had no effect on glucagon release demonstrating an improved therapeutic potential for the treatment of type 2 diabetes.

biological chemistry

Effects of gastric inhibitory polypeptide (GIP) and related analogues on glucagon release at normo- and hyperglycaemia in Wistar rats and isolated islets