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Rosiglitazone stimulates the release and synthesis of insulin by enhancing GLUT-2, glucokinase and BETA2/NeuroD expression |
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| Authors: | Kim Hyo-Sup Noh Jung-Hyun Hong Seung-Hyun Hwang You-Cheol Yang Tae-Young Lee Myung-Shik Kim Kwang-Won Lee Moon-Kyu |
| Affiliation: | a Division of Endocrinology and Metabolism, Samsung Biomedical Research Institute (SBRI), Seoul, Republic of Korea b Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Kangnam-ku, Seoul, Republic of Korea c Division of Endocrinology, Department of Internal Medicine, Inje University College of Medicine, Gyunggi-Do, Republic of Korea |
| Abstract: | Peroxisome proliferator-activated receptor (PPAR)-γ is a member of the nuclear receptor superfamily, and its ligands, the thiazolidinediones, might directly stimulate insulin release and insulin synthesis in pancreatic β-cells. In the present study, we examined the effects of rosiglitazone (RGZ) on insulin release and synthesis in pancreatic β-cell (INS-1). Insulin release and synthesis were stimulated by treatment with RGZ for 24 h. RGZ upregulated the expressions of GLUT-2 and glucokinase (GCK). Moreover, it was found that RGZ increased the expression of BETA2/NeuroD gene which could regulate insulin gene expression. These results suggest that RGZ could stimulate the release and synthesis of insulin through the upregulation of GLUT-2, GCK, and BETA2/NeuroD gene expression. |
| Keywords: | PPAR-γ Rosiglitazone (RGZ) GLUT-2 Glucokinase (GCK) BETA2/NeuroD Glucose stimulated insulin release (GSIR) Insulin synthesis |
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