INS and Hyperglycemia: There are clear similarities between this work and our previous model [10], in that both predict the eventual fast acceleration of the development of diabetes once insulin hypersecretion slows down, and both account for the bistability of achievable compensation (in case of normoglycemia and/or maintained pancreatic reserve) or development of disease (in case of prolonged hyperglycemia with reserve exhaustion due to glucotoxicity).