Abstract
ObjectiveDietary intervention is a practical prevention strategy for age-related hearing loss (AHL). Omega-3 (n-3) polyunsaturated fatty acids (PUFAs) may be effective in prevention of AHL due to their anti-inflammatory and tissue-protective functions. Age-related changes in the hearing function of wild-type and Fat-1 transgenic mice derived from the C57BL/6N strain, which can convert omega-6 PUFAs to n-3 PUFAs and consequently produce enriched endogenous n-3 PUFAs, were investigated to test the efficacy of n-3 PUFAs for AHL prevention.ResultsAt 2 months, the baseline auditory brainstem response (ABR) thresholds were the same in Fat-1 and wild-type mice at 8–16 kHz but were significantly higher in Fat-1 mice at 4 and 32 kHz. In contrast, the ABR thresholds of Fat-1 mice were significantly lower at 10 months. Moreover, the ABR thresholds of Fat-1 mice at low-middle frequencies were significantly lower at 13 months (12 kHz). Body weights were significantly reduced in Fat-1 mice at 13 months, but not at 2, 10, and 16–17 months. In conclusion, enriched endogenous n-3 PUFAs produced due to the expression of the Fat-1 transgene partially alleviated AHL in male C57BL/6N mice.
Highlights
Age-related hearing loss (AHL) is the most common cause of sensorineural hearing loss in adults and is one of the most prevalent age-related physical conditions [1, 2]
There were no differences in the auditory brainstem response (ABR) thresholds in response to 8, 12, or 16-kHz stimuli, the ABR thresholds were significantly higher in response to 4-kHz and 32-kHz stimuli in Fat-1 mice at 2 months (Fig. 1b)
We found that enriched endogenous n-3 polyunsaturated fatty acid (PUFA) suppressed age-related body weight gain and partially slowed the progression of AHL in male C57BL/6N mice
Summary
Time course of ABR thresholds and body weights The C57BL/6N mice exhibit early onset and progression of AHL mainly due to a single nucleotide variant in the Cdh gene (Cdh23753A) [14, 15]. To determine the effects of enriched endogenous n-3 PUFAs on AHL progression, ABR thresholds were first measured at 2, 13, and 16–17 months of age (Fig. 1a). ABR thresholds for both WT and Fat-1 mice were increased compared to those of other groups (13 and 16–17 months) due to unknown reasons, we found that the ABR thresholds were significantly different between the two strains at 10 months (Fig. 2a, Additional file 1: Tables S1). These results suggest that enriched endogenous n-3 PUFAs delayed the early progression of AHL. No apparent differences in age-related cochlear degeneration were found between WT and Fat-1 mice at 13 months
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