These findings are in contrast to our own previously-published results with islets from LepOb/Ob mice in the BTBR strain background – a very robust model of T2D caused by β-cell dysfunction and loss of functional β-cell mass that occurs with 100% penetrance by 10 weeks of age.3,7 In the C57Bl/6J LeptinOb line, it is possible chronic hyperglycemia, over time, would lead to enhanced PGE2 synthetic gene expression and up-regulated agonist-dependent EP3 signaling. The gene discussed is PTGER3; the disease is type 2 diabetes mellitus.