Furthermore, increased HbA1c% was strongly associated with a decline in IENFD and thermal hyperalgesia (Figures 7(a) and 7(e)) also independent of insulin dose (Table 2), indicating that in this rat model of T2D, hyperglycemia contributes to the development of peripheral nerve fiber damage and that glycemic control to some extent may attenuate these damages, as also observed in more recent human studies [23, 24]. This evidence concerns the gene INS and type 2 diabetes mellitus.