Fig. 1. Pioglitazone (Pio) improves palmitate (PA)-induced β-cell impairment via repression of the inflammatory response and endoplasmic reticulum (ER) stress. (A) Mouse insulinoma 6 (MIN6) cells were incubated with 0.5 mM PA in the presence or absence of 10 µM Pio for 24 hours, and the glucose-stimulated (1 or 4.5 g/L) insulin secretion of MIN6 cells was evaluated. Secreted insulin was measured by a mouse insulin enzyme-linked immunosorbent assay (ELISA) kit. The values are representative of 6 independent experiments. (B) Expression of cleaved caspase-3 (c-casp3), an apoptotic protein, was measured by Western blot analysis. (C) Poly (adenosine diphosphate [ADP]-ribose) polymerase (PARP) activity is represented as the percentage of relative absorbance compared to the vehicle group. (D) Transcription of tumor necrosis factor α (TNFA), interleukin 6 (IL6), and IL1B was measured by real time reverse-transcription polymerase chain reaction, and normalized with β-actin. (E) The ER stress proteins, including phosphor-eukaryotic translation initiation factor 2α (p-eIF2α), glucose-regulated protein 78 (GRP78), cleaved-activating transcription factor 6 (c-ATF6), and C/EBP homologous protein (CHOP), were measured by Western blot analysis and (F) the ratio of p-eIF2α, GRP78, and CHOP to β-actin was described. Each value represents the mean of three experiments. t-casp3, total caspase-3; Veh, vehicle; PA, palmitate. ^aP<0.01, ^bP<0.001 compared with the vehicle group; ^cP<0.05, ^dP<0.001 compared with the PA group.