INS and Impaired glucose tolerance: In conclusion, in a state of deficient ERAD capacity, the combined impact of a diminution of mature β cells, an increase in islet β cell phospho-eIF2α with diminished proinsulin synthesis, and enhanced autophagic clearance results in a diminished level of proinsulin that results in markedly decreased insulin content with impaired glucose tolerance (Figure 1, A–C).