The glucose homeostasis is essential for brain function, and energy deficiency is a key feature of brain aging. We investigated whether improving glucose metabolism in the auditory cortex can delay the aging of auditory function of guinea pigs with age-related hearing loss (ARHL) by d-galactose. Auditory function was assessed by auditory brainstem response (ABR), glucose metabolism was detected by micro PET/CT, and the proteome were identified in auditory cortex by two-dimensional electrophoresis and matrix assisted laser desorption/ionization mass spectrometry. Glucose metabolism decreased in the auditory cortex of d-galactose group, and improving glucose metabolism can delay the aging of auditory function by upregulating seven metabolism-related proteins including ATP synthase subunit beta, triosephosphate isomerase, creatine kinase U-type, pyruvate dehydrogenase E1 component subunit beta, alpha-enolase, phosphoglycerate kinase, and tubulin beta-2A chain. These results suggest that the decrease of glucose metabolism in the auditory cortex may be an important role in the aging of auditory function, and improving glucose metabolism in the auditory cortex can delay the aging of auditory function of guinea pig with ARHL induced by d-galactose.

葡萄糖稳态对大脑功能至关重要，而能量缺乏是大脑衰老的一个关键特征。我们研究了改善听觉皮层中的葡萄糖代谢是否可以通过d-半乳糖延缓年龄相关性听力损失 (ARHL) 豚鼠听觉功能的老化。通过听觉脑干反应（ABR）评估听觉功能，通过微型PET/CT检测葡萄糖代谢，通过二维电泳和基质辅助激光解吸/电离质谱法鉴定听觉皮层中的蛋白质组。d听觉皮层的葡萄糖代谢降低-半乳糖基团，改善葡萄糖代谢可通过上调ATP合酶β亚基、磷酸丙糖异构酶、肌酸激酶U型、丙酮酸脱氢酶E1成分亚基β、α-烯醇化酶、磷酸甘油酸激酶等7种代谢相关蛋白来延缓听觉功能老化和微管蛋白β-2A 链。这些结果提示听觉皮层糖代谢的降低可能是听觉功能老化的重要作用,改善听觉皮层糖代谢可延缓d-半乳糖诱导的ARHL豚鼠听觉功能的老化。.