Retinopathy is a leading cause of blindness, and there is currently no cure. Earlier identification of the progression of retinopathy could provide a better chance for intervention. Diet has profound effects on retinal function. A maternal high fructose diet (HFD) triggers diseases in multiple organs. However, whether maternal HFD impairs retinal function in adult offspring is currently unknown. By using the rodent model of maternal HFD during pregnancy and lactation, our data indicated a reduced b-wave of electroretinography (ERG) in HFD female offspring at 3 months of age compared with age-matched offspring of dams fed regular chow (ND). Immunofluorescence and Western blot analyses indicated that the distributions and expressions of synaptophysin, postsynaptic density protein 95 (PSD95), and phospho(p)-Ca²⁺/calmodulin-stimulated protein kinase IIa (CaMKIIa) were significantly suppressed in the HFD group. Furthermore, the ATP content and the mitochondrial respiratory protein, Mt CPX 4-2, were decreased. Moreover, the expressions of peroxisome proliferator-activated receptor g coactivator 1-α (PGC-1α) and mitochondrial transcription factor A (TFAM) in the retina of the HFD group were downregulated. Treatment with coenzyme Q₁₀ (Q10), a key mediator of the electron transport chain, effectively reversed these abovementioned dysfunctions. Together, these results suggested that maternal HFD impaired retinal function in adult female offspring. The mechanism underlying early-onset retinopathy may involve the reduction in the capacity of mitochondrial energy production and the suppression of synaptic plasticity. Most importantly, mitochondria could be a feasible target to reprogram maternal HFD-damaged retinal function.

中文翻译：

---

母体高果糖饮食通过抑制线粒体功能障碍介导的突触可塑性诱导早发性视网膜病变

视网膜病变是导致失明的主要原因，目前无法治愈。早期识别视网膜病变的进展可以提供更好的干预机会。饮食对视网膜功能有着深远的影响。母体高果糖饮食 (HFD) 会引发多个器官的疾病。然而，目前尚不清楚母体 HFD 是否会损害成年后代的视网膜功能。通过在怀孕和哺乳期间使用母体 HFD 的啮齿动物模型，我们的数据表明，与喂食常规饲料 (ND) 的年龄匹配的母猪后代相比，3 个月大的 HFD 雌性后代的视网膜电图 (ERG) 的 b 波减少。免疫荧光和蛋白质印迹分析表明突触素、突触后密度蛋白 95 (PSD95) 和磷酸 (p)-Ca ²⁺的分布和表达在 HFD 组中，/钙调蛋白刺激的蛋白激酶 IIa (CaMKIIa) 受到显着抑制。此外，ATP 含量和线粒体呼吸蛋白 Mt CPX 4-2 减少。此外，HFD组视网膜中过氧化物酶体增殖物激活受体g共激活因子1-α（PGC-1α）和线粒体转录因子A（TFAM）的表达下调。辅酶 Q ₁₀治疗(Q10) 是电子传递链的关键介质，有效地逆转了上述这些功能障碍。总之，这些结果表明母体 HFD 损害了成年雌性后代的视网膜功能。早发性视网膜病变的机制可能涉及线粒体能量产生能力的降低和突触可塑性的抑制。最重要的是，线粒体可能是重新编程母体 HFD 损伤的视网膜功能的可行目标。