Distinction between auditory electrophysiological responses in type 1 and type 2 diabetic animal models.

Neurological research has focused recently on determining the molecular mechanisms of common causes of damage to the peripheral and central nervous systems. One of the metabolic systemic diseases that can result in sensorineural hearing loss is diabetic mellitus (DM). In this study, we aimed to compare the auditory electrophysiological responses present in animal models of type 1 and type 2 DM using auditory brainstem response (ABR), auditory middle latency response (AMLR), and transient evoked otoacoustic emission (TEOAE) in animal model. We found that ABR threshold shifts and latency delays were similar in both types of DM. On the other hand, we found that type 2 diabetic mice exhibited more severe dysfunction to the central auditory pathway, as measured AMLRs and the cochlear hair cells, as measured TEOAEs. These results together suggest that hyperglycemia associated with type 1 or type 2 DM causes auditory nerve dysfunction, while hyperinsulinemia associated with type 2 DM causes dysfunction to both the central auditory pathways and cochlear hair cells.