Vitamin D deficiency—a new cause of cochlear deafness

Brookes, G. B.

doi:10.1017/s0022215100094330

Cited by 51 publications

(29 citation statements)

References 43 publications

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“…Our finding of VDR expression in the mouse cochlea implies that vitamin D is potentially important in maintaining hearing, which is in agreement with the previous reports [Brookes and Morrison, 1981;Brookes, 1983Brookes, , 1985Ziporyn, 1983]. Although VDR protein was not detected in the VDR KO mouse cochlea, which is at odds with reports on a truncated form of VDR in the same strain of VDR KO mice [Bula et al, 2005], this Caspase 3 activation was decreased in the cochlea of VDR KO, compared to the WT mice.…”

Section: Discussionsupporting

confidence: 91%

“…Vitamin D deficiency is a common factor in the reduction of bone-mineral density, and is associated with an increased risk of several chronic age-related diseases [Javaid et al, 2006;Zittermann, 2003]. Vitamin D deficiency, VDR malfunction, hypoparathyroidism, and hypervitaminosis have long been suggested to be potential causes of sensorineural hearing loss [Brookes and Morrison, 1981;Brookes, 1983Brookes, , 1985Cohen et al, 1979;Ikeda et al, 1989Ikeda et al, , 1987Ishida et al, 2001;Ziporyn, 1983].…”

mentioning

confidence: 99%

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Progressive Hearing Loss in Mice with a Mutated Vitamin D Receptor Gene

Zou¹,

Minasyan

Keisala

et al. 2008

Audiol Neurotol

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Background: Both hypo- and hypervitaminosis D can cause sensorineural hearing loss, and aural symptoms due to vitamin D insufficiency are especially common during gravidity. Hormonal forms of vitamin D regulate transcription by binding with the high-affinity vitamin D receptor (VDR). Objective: To assess the effects of impaired vitamin D action in VDR knockout (KO) mice on hearing, cochlear morphology, and cochlear gene expression. Materials and Methods: Eighteen young male and female mice (10 VDR KO and 8 wild type, WT, ≤6 months old), 33 adult male and female mice (16 VDR KO and 17 WT, between 7 and 14 months old), and 11 aged male and female mice (5 VDR KO and 6 WT, ≧15 months old) on 129S1 genetic background were studied. Auditory thresholds were evaluated by auditory brain stem response. Morphological changes were analyzed using plastic embedding and light microscopy. The expression of key genes (known to play a role in the regulation of cochlear function), and caspase 3 activity, were assessed using immunofluorescent confocal microscopy. Results: There was a statistically significant difference between the young and the adult groups, and between the adult and aged groups of WT mice. There was also a statistically significant difference between the adult and aged groups in VDR KO mice, and between the young WT group and the young VDR KO group. Spiral ganglion cell loss was observed in the basal turn of adult VDR KO mice, a phenomenon infrequently found in WT mice. Expression of connexin 26, KCNJ10, and transient receptor potential channel vanilloid subfamily 4/6 was not affected by VDR KO-mediated hearing loss. Caspase 3 activation was detected in the spiral ganglion cell and its satellite cells, stria vascularis, spiral ligament fibrocytes, and the organ of Corti in both genotypes. However, the percentage of positive cells and the staining intensity were lower in the VDR KO (compared to the WT) mice. Conclusion: These data suggest that sensorineural hearing loss progressively developed at an earlier age in VDR KO mice. While the fundamental gene expressions in the cochlea were not influenced by VDR mutation, it resulted in decrease of caspase 3 activation, which may be one of the factors underlying accelerating age-related hearing loss observed in VDR KO mice.

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

Progressive Hearing Loss in Mice with a Mutated Vitamin D Receptor Gene

Zou¹,

Minasyan

Keisala

et al. 2008

Audiol Neurotol

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“…For example, VDR is also widely distributed throughout the olfactory system [23], indirectly supporting the possibility that vitamin D and VDR may modulate olfaction. Likewise, VDR genetic partial ablation leads to hearing defects in mice [24], consistent with clinical data [25,26] on hearing deficits associated with vitamin D dysfunctions [27]. Other recent data have shown that in some tissues vitamin D up-regulates transient receptor potential (TRP) vanilloid calcium-selective cation channels, such as TRPV5 and TRPV6 [28,29].…”

Section: Introductionsupporting

confidence: 62%

Neophobia, sensory and cognitive functions, and hedonic responses in vitamin D receptor mutant mice

Minasyan

Keisala

Lou

et al. 2007

The Journal of Steroid Biochemistry and Molecular Biology

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“…Auditory dysfunction has been associated with deficiencies of several micronutrients in humans (6)(7)(8)(9) and young growing animals (10)(11)(12)(13)(14). However, we found no studies in humans or experimental animals that specifically examined the role of nutrition in age-related hearing loss.…”

Section: Introductionmentioning

confidence: 85%

Age-related hearing loss, vitamin B-12, and folate in elderly women

Houston

Johnson

Nozza

et al. 1999

The American Journal of Clinical Nutrition

116

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Background: Hearing impairment is 1 of the 4 most prevalent chronic conditions in the elderly. However, the biological basis of age-related hearing loss is unknown. Objective: The objective was to test the hypothesis that agerelated hearing loss may be associated with poor vitamin B-12 and folate status. Design: A thorough audiometric assessment was conducted in 55 healthy women aged 60-71 y. Hearing function was determined by the average of pure-tone air conduction thresholds at 0.5, 1, 2, and 4 kHz and was categorized into 2 groups for logistic regression analyses: normal hearing (< 20 dB hearing level; n = 44) and impaired hearing (≥ 20 dB hearing level; n = 11). Results: Mean age was the same (65 y) for the normal hearing and impaired hearing groups. Pure-tone averages were inversely correlated with serum vitamin B-12 (r = Ϫ0.58, P = 0.0001) and red cell folate (r = Ϫ0.37, P = 0.01). Women with impaired hearing had 38% lower serum vitamin B-12 (236 compared with 380 pmol/L, respectively, P = 0.008) and 31% lower red cell folate (425 compared with 619 nmol/L, respectively, P = 0.02) than women with normal hearing. Among participants who did not take supplements containing vitamin B-12 or folate, women with impaired hearing had 48% lower serum vitamin B-12 (156 compared with 302 pmol/L, respectively, P = 0.0007) and 43% lower red cell folate (288 compared with 502 nmol/L, respectively, P = 0.001) than women with normal hearing. Conclusion: Poor vitamin B-12 and folate status may be associated with age-related auditory dysfunction.Am J Clin Nutr 1999;69:564-71.

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Vitamin D deficiency—a new cause of cochlear deafness

Cited by 51 publications

References 43 publications

Progressive Hearing Loss in Mice with a Mutated Vitamin D Receptor Gene

Progressive Hearing Loss in Mice with a Mutated Vitamin D Receptor Gene

Neophobia, sensory and cognitive functions, and hedonic responses in vitamin D receptor mutant mice

Age-related hearing loss, vitamin B-12, and folate in elderly women

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