Abstract
Objective:
Previous studies have shown that
hearing function is also vulnerable to the effects of
diabetes mellitus which can be shown by
brainstem auditory evoked potential and distortion product otoacoustic emission recordings. This study aimed to investigate the changes of
brainstem auditory evoked potential and distortion product otoacoustic emission in
hyperglycemia and whether there is a relationship between reactive
oxygen substances
production and
hearing deterioration in the
rat model.
Methods:
25
streptozotocin induced diabetic
rats were divided into three groups control, high
blood glucose, and
diabetes mellitus.
Brainstem auditory evoked potential and distortion product otoacoustic emission were recorded, and
thiobarbituric acid reactive substances levels were measured in the
brainstem tissue.
Results:
At 8 kHz, the latencies of I, II, III, IV, and V
brainstem auditory evoked potential waves in high
blood glucose and
diabetes mellitus groups were elongated, at 16 kHz, only these
wave latencies of the
diabetes mellitus group were prolonged compared with the
control group. A significant decrease was also found in distortion product otoacoustic emission amplitudes at 4, 6, 8, and 10 kHz in the high
blood glucose and
diabetes mellitus groups compared to the
control group. There was a significant increase in
thiobarbituric acid reactive substances values due to the increase in
blood glucose levels in the high
blood glucose and
diabetes mellitus groups compared to the
control group.
Conclusion:
These results suggested that high
blood glucose levels may cause
hearing impairment not only in the diabetic
state but also in the period of
hyperglycemia before the onset of manifest
diabetes mellitus and reactive
oxygen substances may
play an important
role in the pathophysiology of
diabetes mellitus. We suggest that regulating high
glucose levels even before the onset of manifest
diabetes mellitus may prevent hazardous effects on
hearing function. Level of evidence Level 3.