PMC

Recovery from noise-induced injury was significantly impaired in diabetic mice at 4 and 8 kHz. The time course of ABR threshold shifts at each frequency in diabetic (DM) (n = 4) and control (Ctrl) (n = 4) groups after noise exposure (4-kHz OBN, 105-dB SPL for 2 h) (A–D). Data are means ± SE. *P < 0.05 diabetic vs. control group.

The cochlear blood flow ratio measured by laser-Doppler flowmeter is shown for both diabetic (DM) (n = 4) and control (Ctrl) (n = 4) mice 14 days after noise exposure (4-kHz OBN, 105-dB SPL for 2 h) as described in . Data are means ± SE. **P < 0.01 diabetic vs. control group.

Time course of changes in body weight (A) and blood glucose level (B) at baseline (n = 15 each for diabetic [DM] and control [Ctrl]) and 1 month (n = 15 each for diabetic and control), 3 months (n = 10 each for diabetic and control), and 5 months (n = 5 each for diabetic and control) after induction of diabetes. Data are means ± SE. **P < 0.01, ***P < 0.001 diabetic vs. control group.

Chronologic changes in the ABR threshold shift were not significantly different between the diabetic group and controls throughout the observation period except at 4 kHz at 1 month. The time course of ABR threshold shifts compared with baseline (A–C) at each observation period (1, 3, and 5 months) for the diabetic (DM) group (n = 5 for each period) and control (Ctrl) group (n = 5 for each period). Data are means ± SE. *P < 0.05 diabetic vs. control group.

A and B: Whole cochleae (top panels; scale bar = 100 μm) and SGCs in the apical turn of the cochleae (bottom panels; scale bar = 50 μm) 14 days after noise exposure (4-kHz OBN, 105-dB SPL for 2 h). H-E staining of control [Ctrl] cochlea (A) and diabetic (DM) cochlea (B). Means of the densities of spiral ganglion neurons 14 days after noise exposure are shown in C (n = 4 for each group). Data are means ± SE. *P < 0.05, **P < 0.01 diabetic vs. control group. (A high-quality digital representation of this figure is available in the online issue.)

H-E staining (top panel; scale bar = 100 μm) and CD31 immunostaining (bottom panel; scale bar = 20 μm) of the vessel endothelial cells at the modiolus in control (Ctrl) cochlea (A) and diabetic (DM) cochlea (B). The vessel wall thickness of staining for CD31, quantified by a computer-aided image-analysis system, is shown for both diabetic (n = 5) and control (n = 5) mice at 5 months of diabetes as described in (C). Data are means ± SE. **P < 0.01 diabetic vs. control group. (A high-quality digital representation of this figure is available in the online issue.)