Lipidomics profiling identifies β-oxidation as a key process in noise-induced hearing loss

Area of Science:

• Oto-neurology
• Metabolomics
• Biochemistry

Background:

• Noise-induced hearing loss (NIHL) is a significant global health issue, particularly affecting young adults.
• The molecular mechanisms underlying NIHL and effective pharmacological treatments remain largely unknown.
• Current understanding of cochlear energy metabolism during noise exposure is limited.

Purpose of the Study:

• To investigate the metabolic changes in the inner ear following noise exposure.
• To explore the role of fatty acid oxidation in NIHL.
• To evaluate the potential of targeting cochlear energy metabolism for NIHL prevention.

Main Methods:

• Utilized targeted and untargeted lipidomics to analyze inner ear metabolic profiles after noise exposure.
• Administered Etomoxir, a β-oxidation inhibitor, to assess its effects on hearing and cochlear metabolism.
• Quantified hearing loss following intense noise exposure in both control and treated groups.

Main Results:

• Noise exposure significantly altered fatty acid and acylcarnitine species in the inner ear, indicating increased β-oxidation.
• Inhibition of β-oxidation with Etomoxir did not impair hearing in normal conditions.
• Etomoxir treatment significantly reduced the degree of hearing loss after intense noise exposure.

Conclusions:

• Noise exposure triggers specific metabolic shifts in the cochlea, notably enhancing β-oxidation.
• Modulating cochlear energy metabolism, specifically by inhibiting β-oxidation, offers a potential therapeutic strategy for NIHL.
• These findings provide novel insights into the metabolic underpinnings of NIHL and suggest new avenues for treatment.