![]() ![]() The role of the cochlea as a direct target organ for insulin action has not been well characterized. 12 Thus, a number of studies are in agreement with reports showing harmful effects of induced hyperinsulinemia on inner ear metabolic and ion homeostasis. 11 In humans, insulin resistance, impaired fasting glucose and beta-cell dysfunction have been reported as independent risk factors for hearing impairment even before the onset of type 2 diabetes. 10 Furthermore, hyperinsulinemia, a marker for insulin resistance and type 2 diabetes, has been suggested to explain differences in dysfunction of specific auditory pathways in the two types of diabetes in a comprehensive neuro-electrophysiological study in mice. ![]() ![]() The progression of hearing loss in mice with type 1 diabetes induced with streptozotocin or type 2 diabetes induced with high fat die (HFD), respectively, has been reported to have different characteristics as measured by auditory brain stem response and distortion products otoacustic emissions (DPOAE). 1–5 Although several theories have been proposed (eg, microangiopathy, advanced glycation end products, reactive oxidative stress and mitochondrial dysfunction, demyelination of the auditory nerve, spiral ganglion loss and atrophic changes of organ of Corti cells 5–9), the exact underlying mechanisms responsible for diabetes-induced damage to the auditory system remain uncertain. Ample evidence shows that type 1 and type 2 diabetes negatively impact on the function of the vestibular and auditory systems both in humans and in animal models. ![]()
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