gms | German Medical Science

Epidemiological data indicate an excess incidence of sensorineural hearing loss in patients with diabetes mellitus. However, the pathophysiological background of this diabetic otopathy remains unclear. We investigated hearing function (AEPs) and inner ear morphology (electron microscopy) and in parallel kidney function and morphology in the Zucker diabetic fatty (ZDF) rat, a type 2 diabetic animal model. Homozygous (ZDF fa/fa, n=8), diabetic animals had developed overt diabetes mellitus (HbA1c > 10 % by age 15 weeks) and progressive albuminuria (24.4+/-4.9 mg/h/kg at age 42 weeks), whereas heterozygous, non-diabetic littermates (n=9) remained normoglycaemic and did not develop albuminuria. At age 42 weeks, the hearing threshold was increased in the diabetic animals to 45.0+/-2.1 dB, compared to 34.7+/-1.0 in non-diabetic rats (p<0.05). Diabetic nephropathy and otopathy developed in parallel, as reflected by the linear correlation between albuminuria and hearing threshold in the diabetic animals (r=0.65, p<0.05). Histological and electron microscopic analysis demonstrated all typical features of diabetic nephropathy in the homozygous rats (glomerulosclerosis, podocyte damage, and tubular degeneration). Morphological analysis of the inner ear did not reveal microvascular injury. However, severe degenerative damage was found in the intermediate cells of the stria vascularis. Conclusion: Type 2 diabetes mellitus is associated with functional and morphological damage to the inner ear, which occurs in parallel to typical end organ damage, such as diabetic nephropathy. In contrast to the microvascular injury in nephropathy, diabetic otopathy is characterized by a specific damage to the intermediate cells of the stria vascularis.