title: Increased inner ear susceptibility to noise injury in mice with streptozotocin-induced diabetes.
abstract: We aimed to investigate the pathophysiology of diabetes-associated hearing impairment in type 1 diabetes using mice with streptozotocin-induced diabetes (C57BL/6J; male). Hearing function was evaluated 1, 3, and 5 months after induction of diabetes (five diabetic and five control animals per time point) using auditory-evoked brain stem responses (ABRs). Mice (four diabetic and four control) were exposed to loud noise (105 dB) 5 months after induction of diabetes. ABRs were measured before and after noise exposure. Cochlear blood flows were measured by laser-Doppler flowmeter. Spiral ganglion cells (SGCs) were counted. Vessel endothelial cells were observed by CD31 immunostaining. Chronologic changes in the ABR threshold shift were not significantly different between the diabetic and control groups. However, vessel walls in the modiolus of the cochleae were significantly thicker in the diabetic group than the control group. Additionally, recovery from noise-induced injury was significantly impaired in diabetic mice. Reduced cochlea blood flows and SGC loss were observed in diabetic mice cochleae after noise exposure. Our data suggest that diabetic cochleae are more susceptible than controls to loud noise exposure, and decreased cochlear blood flow due to sclerosis of the vessels and consequent loss of SGCs are possible mechanisms of hearing impairment in diabetic patients.
authors.affiliation: Department of Otolaryngology–Head and Neck Surgery, Kobe University Graduate School of Medicine, Kobe, Japan. fujitake@med.kobe-u.ac.jp
authors.forename: Takeshi
authors.initials: T
authors.lastname: Fujita
authors.forename: Daisuke
authors.initials: D
authors.lastname: Yamashita
authors.forename: Sayaka
authors.initials: S
authors.lastname: Katsunuma
authors.forename: Shingo
authors.initials: S
authors.lastname: Hasegawa
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Tanimoto
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Nibu
mesh_terms: D000818:Animals; D002452:Cell Count; D003051:Cochlea / Q000098:blood supply / Q000473:pathology; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D004198:Disease Susceptibility; D007758:Ear, Inner / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology*; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D016057:Evoked Potentials, Auditory, Brain Stem; D006317:Hearing Loss, Noise-Induced / Q000150:complications* / Q000534:rehabilitation; D017078:Laser-Doppler Flowmetry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008833:Microcirculation; D055806:Microvessels / Q000473:pathology / Q000503:physiopathology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D011897:Random Allocation; D012598:Sclerosis; D013136:Spiral Ganglion / Q000473:pathology; D013311:Streptozocin
chemical_list: D019408:Platelet Endothelial Cell Adhesion Molecule-1; D013311:Streptozocin