Role of Islet Glucokinase, Glucose Metabolism, and Insulin Pathway in the Enhancing Effect of Islet Neogenesis-Associated Protein on Glucose-Induced Insulin Secretion
; Román, Carolina Lisi
; Barbosa Sampaio, Helena C. ; Boschero, Antonio C. ; Gagliardino, Juan Jose 
Otros responsables
Fecha
08/2015
Editorial
Lippincott Williams
Revista
Pancreas
Título del libro
Nombre del evento
Fecha del evento
Institución organizadora
ISSN
0885-3177
eISSN
1536-4828
ISBN
Idioma
Inglés
Tipo del evento
Clasificación temática
Palabras clave
Resumen
Objective: To demonstrate the role of islet glucokinase, glucose metabolism, and intracellular insulin mediators in the enhancing effect of islet neogenesis-associated protein pentadecapeptide (INGAP-PP) on glucoseinduced insulin secretion.
Methods: Islets from normal rats were cultured for 4 days in the absence or presence of 10 μg/mL INGAP-PP, with/without Wortmannin or LY294002. Islets were incubated with different glucose concentrations to measure insulin secretion and content, hexokinase and glucokinase activity, glucose oxidation and utilization, glucokinase, insulin receptor, insulin receptor substrate (IRS)-1/2, and PI3K concentration and phosphorylation.
Results: The INGAP-PP significantly increased insulin release at high but not at low glucose concentration, glucokinase activity, glucose metabolism, glucokinase, insulin receptor, IRS-2 and PI3K protein concentration, insulin receptor and IRS-1/2 tyrosine phosphorylation, and the association of p85 with IRS-1. Wortmannin and LY294002 blocked INGAP-PP effect on insulin secretion and glucokinase protein levels in a dosedependent manner.
Conclusions: The enhancing effect of INGAP-PP on glucose-induced insulin release could be partly ascribed to its effect on glucokinase activity and glucose metabolism and is mainly mediated by the PI3K/AKT pathway. These results, together with the low hypoglycemia risk associated with the use of INGAP-PP, offer a new alternative for diabetes prevention and treatment.
Colecciones
Aprobación
Revisión
Complementado por
Referenciado por
Licencia Creative Commons
Excepto donde se indique lo contrario, la licencia de este ítem se describe como by-nc-sa
