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Hearing Loss and Cochlear Pathology in a Type II Diabetic Mouse Model
Author(s) -
Miller Sean,
Boettcher Flint,
Phillips Grady,
Anne Gratton Michael
Publication year - 2011
Publication title -
otolaryngology–head and neck surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.232
H-Index - 121
eISSN - 1097-6817
pISSN - 0194-5998
DOI - 10.1177/0194599811415823a261
Subject(s) - spiral ganglion , hearing loss , cochlea , auditory brainstem response , ultrastructure , hair cell , inner ear , endocrinology , pathology , medicine , diabetes mellitus , wild type , type 2 diabetes , biology , anatomy , mutant , audiology , genetics , gene
Objective 1) Determine whether a type II diabetic mouse model demonstrates hearing loss. 2) Examine cochlear ultrastructure of a type II diabetic mouse model for evidence of pathology. Method The Lepr db /Lepr db (db/db) mouse has a leptin receptor point mutation which manifests as polyphagia, hyperglycemia, and obesity, mimicking type II diabetes. Db/db and wild type mice from the parent strain underwent auditory brainstem response measurements followed by cochlear ultrastructure analysis using scanning and transmission electron microscopy. Results At 12 weeks of age, the mutant animals demonstrate a profound hearing loss from 8 to 32 kHz, which is in contrast to published data of a 10 dB shift at 8 kHz and 30 dB shift at 16 to 32 kHz for age‐matched, wild type C57BL/6J counterparts. In addition, fine structure analysis reveals evidence of morphological alterations in multiple locations within the cochlea, including loss of neuron density in the spiral ganglion, stria vascularis edema, and endothelial abnormalities within strial capillaries. Age‐matched controls are without similar ultrastructural changes. Scanning electron microscopy reveals no evidence of hair cell loss or other identifiable abnormalities. Conclusion This is the first demonstration of cochlear pathophysiology in a genetically derived type II diabetic mouse model. Use of the db/db mouse provides an opportunity to investigate the underlying mechanism of type II diabetes associated hearing loss.

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