J Korean Diabetes Assoc.
2003 Jun;27(3):241-252.
Effects of Peroxisome Proliferator-activated Receptor-gamma(PPARgamma) on the Pancreatic beta Cell Proliferation
- Affiliations
-
- 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Ilsan-Paik Hospital, Inje University College of Medicine, Korea.
- 2Division of Endocrinology and Metabolism, Department of Internal Medicine, Hae-nam hospital, Korea.
- 3Division of Endocrinology and Metabolism, Department of Internal Medicine, Hangang Sacred Heart hospital, Hanllym University College of Medicine, Korea.
- 4Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University of Medicine, Seoul, Republic of Korea.
Abstract
-
BACKGROUND: The effects and mechanisms of PPARgamma ligands on the cell proliferation in pancreatic beta cells were examined.
METHODS
PPARgamma 1 cDNA was overexpressed in INS-1 cells using an adenoviral vector. The cell proliferations were measured by the MTT assay method, following the treatments with troglitazone (TGZ), rosiglitazone (RGZ), 15d-prostaglandin J2 (15d-PGJ2) or retinoic acid (RA), at increasing doses, in INS-1 and PPARgamma overexpressed INS-1 cells. The apoptosis, telomere length and cell cycles were determined after the PPARgamma ligand treatment.
RESULTS
The long-term incubation, with PPARgamma ligands over 24 hr, inhibited the INS-1 cell proliferation rate. Apoptosis was not observed with the PPARgamma ligand treatment. G1 cell cycle arrest was observed with the troglitazone treatment. The telomere length remained unchanged following the TGZ treatment. The basal cell proliferation rate was unaffected by the overexpression of PPARgamma . After 48 h of TGZ treatment, the proliferation of the INS-1 cells was inhibited, in a dose- dependent manner, both with and without the overexpression. Moreover, the degree of inhibition was exaggerated in the PPARgamma overexpressed cells compared to beta gal overexpressed cells.
CONCLUSION
PPARgamma ligands have direct inhibitory effects on the proliferation of INS-1 cells. Although the basal cell proliferation rate was not affected by PPARgamma overexpression, the PPARgamma overexpression and PPARgamma ligands have a synergistic inhibitory effect on the cell proliferation rate in pancreatic beta cells. G1 cell cycle arrest may be involved in the reduction of cell proliferation due to PPARgamma ligands.
- Full Text Links
-
- Actions
-
Cited
- CITED
-
- Close
- Share
-
- Similar articles
-
- Effects of Sulfonylureas on Peroxisome Proliferator-Activated Receptor gamma Activity and on Glucose Uptake by Thiazolidinediones
- The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-gamma in Vascular Smooth Muscle Cells
- Change of peroxisome proliferator-activated receptor gamma expression pattern in the gerbil dentate gyrus after transient global cerebral ischemia
- Ciglitazone, a Peroxisome Proliferator-Activated Receptor Gamma Ligand, Inhibits Proliferation and Differentiation of Th17 Cells
- Fenofibrate, a peroxisome proliferator-activated receptor alpha-agonist, blocks lipopolysaccharide-induced inflammatory pathways in mouse liver
