PPARδ Activation Rescues Pancreatic β-Cell Line INS-1E from Palmitate-Induced Endoplasmic Reticulum Stress through Enhanced Fatty Acid Oxidation
Figure 3
PPARδ protects pancreatic β cells from palmitate-induced lipotoxicity. (a) INS-1E cells were treated with 0.5 mM palmitate alone, combination of 0.5 mM palmitate and 100 nM GW501516, combination of 0.5 mM palmitate and 1 μM GSK0660, or combination of 0.5 mM palmitate, 100 nM GW501516, and 50 μm Etomoxir 48 h. Apoptosis was measured by TUNEL assay. (b) Expression of Bcl-2 was examined by Western blot. Upper panal: representative image of immunoblot; pottom panal: statistical analyses of relative densitometric value. (c) INS-1E cells were treated with 0.5 mM palmitate alone, combination of 0.5 mM palmitate, 100 nM GW501516, and 1 μM GSK0660, or combination of 0.5 mM palmitate, 100 nM GW501516, and 50 μm Etomoxir for 48 h. Activity of caspase-3 was examined. (d) INS-1E cells were treated with 0.5 mM palmitate alone, combination of 0.5 mM palmitate, and 100 nM GW501516, or combination of 0.5 mM palmitate and 1 μM GSK0660 for 48 h. BIS and BSIS from INS-1E cells were examined. All the data were from three independent experiments (). : versus untreated group; : versus palmitate-treated group; : versus the group treated with a combination of palmitate and GW501516.
