Figure 5

Activation of GPR40 reduces apoptosis through cAMP and calcium signaling. (A) NIT1 cells were cultured under inflammation conditions with or without GPR40 agonist for 72 h in presence of CaMKII (AIP), Calcineurin (CsA) and soluble ADCY (KH7) inhibitors or cAMP activator (Fsk) as indicated (A). GPR40 agonist and Fsk reduced inflammation induced caspase-3 activity. AIP, CysA and KH7 blocked GPR40 agonist’s ability to reduced caspase-3 activity. (B) After chronic culture for 72 h, NIT1 cells were pre-treated with low glucose containing KRBH followed by treatment for 1 h with low or high glucose and cAMP levels in cells were determined by enzyme immunoassay. (n = 4, *P < 0.05, **P < 0.01, ***P < 0.001).