Overall, we conclude that Cpt1aPdx1−/− mice have several features consistent with eventual development of type 2 diabetes (T2D) e.g., impaired glucose tolerance and increased pancreatic TGs, but no change in islet glucagon abundance or markers of β-cell maturity (e.g., MafA, Pdx1, Nkx6.1), as noted in models of established disease (e.g., db/db mice) (13). This evidence concerns the gene NKX6-1 and type 2 diabetes mellitus.