|Title:||Rosiglitazone (Brl 49653) Enhances Insulin Secretory Response Via Phosphatidylinositol 3-Kinase Pathway||Authors:||TAI, TONG-YUAN
|Keywords:||ACTIVATED RECEPTOR-GAMMA;BETA-CELLS;FATTY RATS;OBESE RATS;THIAZOLIDINEDIONES;ISLETS||Issue Date:||2001||Journal Volume:||v.50||Journal Issue:||n.11||Start page/Pages:||2598-2602||Source:||DIABETES||Abstract:||
To elucidate the direct effect of rosiglitazone (RSG), a new thiazolidinedione antihyperglycemic agent, on pancreatic insulin secretion , an in situ investigation by rat pancreatic perfusion was performed. At a basal glucose concentration of 6 mmol/l, RSG (0.045-4.5 mu mol/l) stimulated insulin release in a dose-dependent manner. In addition, 4.5 mu mol/l RSG potentiated the glucose (10 mmol/ l)-induced insulin secretion. Both the first and second phases of glucose-induced insulin secretion were significantly enhanced by RSG, by 80.7 and 52.4%, respectively. The effects of RSG on insulin secretion were inhibited by a phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002. In contrast, the glucose-stimulated insulin secretion was not affected by LY294002. The potentiation effect of RSG on glucose-stimulated insulin secretion, in both the first and second phases, was significantly blocked by LY294002. These results suggest that RSG has a direct potentiation effect on insulin secretion in the presence of 10 mmol/l glucose, mediated through PI3K activity. The inability of LY294002 to inhibit glucose-induced insulin secretion suggests that different pathways are responsible for glucose and RSG signaling.
|Appears in Collections:||醫學系|
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