Glycative stress and the inner ear disorder

抄録

Sensorineural hearing loss is reported to be frequently associated with diabetic patients; however, it has not been widely recognized as a complication. Renal disorders are well known as one of the three major complications of diabetes, and the renal glomerulus has a histological similarity to the cochlear stria vascularis of the inner ear. It is well known that ototoxicity and nephrotoxicity are common adverse events in administration of aminoglycoside antibiotics and platinum-based antineoplastic agents. As just described, the relationship between inner ear disease and renal disease has been pointed out before. In order to elucidate the mechanism of the onset of hearing loss in diabetes, we conducted a study using Tsumura Suzuki Obese Diabetes (TSOD) mouse, a type 2 diabetes mellitus (T2DM) model. It was confirmed that TSOD mice developed deafness earlier than those of the control, and histopathologically, a significant reduction in the capillary distribution density was observed in the stria vascularis. This is considered to be a finding of diabetic microangiopathy in the inner ear. In order to prevent hearing loss caused by diabetes, caloric restriction and Kampo administration (Bofutsushosan and Daisaikoto) were conducted with TSOD mice, resulting in the hearing loss being significantly ameliorated and the cochlear blood flow being maintained. On the other hand, the administration of metformin, drawing attention in the field of anti-aging medicine, was not effective in TSOD mice, while, in the presbycusis model DBA/2, the hearing loss was suppressed from the early stage in an interesting issue. The background of T2DM is often associated with the metabolic syndrome caused by excessive accumulation of visceral fat. Various factors are involved in its pathogenesis in a complicated manner. Further studies are needed to clarify the mechanism of diabetic inner ear disorder.