BDKRB1 and Insulin resistance: Importantly, the present study confirms the contribution of CPM and excludes the possibility that cathepsin X could intervene in the formation of B1R ligands (Nagler et al., 2010) or that dynorphin could be an endogenous activator of the B1R (Lai et al., 2006, 2008; Lee et al., 2014) in this pro-inflammatory model of insulin resistance.