糖尿病视网膜病变玻璃体代谢缺陷:探索膳食补充解决关键代谢物失衡的潜力。

Clinical ophthalmology (Auckland, N.Z.) Pub Date : 2025-08-27 eCollection Date: 2025-01-01 DOI:10.2147/OPTH.S531638
John Kim Hiller, Elise Sandås Sand, Helge Rootwelt, Anja Østeby Vassli, Xhevat Lumi, Morten Carstens Moe, Tor Paaske Utheim, Katja Benedikte Prestø Elgstøen, Goran Petrovski
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引用次数: 0

摘要

目的:本研究旨在探讨糖尿病视网膜病变(DR)不同阶段的糖尿病患者玻璃体的代谢变化,并探讨可能的饮食干预来减轻这些变化。患者和方法:23例玻璃体切除术患者玻璃体标本分为对照组、糖尿病无DR、非增殖性DR (NPDR)和增殖性DR (PDR)。使用质谱法进行代谢组学分析,重点是识别显著改变的代谢物。结果:共确定了82个特征,其中几个特征与对照组相比显着降低了DR。NPDR组抗坏血酸和牛磺酸显著降低(p < 0.01),胆碱和n -乙酰天冬氨酸显著降低(p < 0.01)。塔格糖显著降低PDR (p < 0.05),水苏氨酸和丝氨酸呈双相趋势,NPDR降低(p < 0.001; p < 0.05), PDR升高(p < 0.05)。结论:研究结果表明,DR患者玻璃体中涉及抗氧化防御、膜完整性和神经元功能的关键代谢物被破坏,针对这些代谢缺陷的饮食补充,如增加抗坏血酸、牛磺酸、丝氨酸、胆碱和水苏氨酸的摄入,可能为控制DR进展提供辅助支持。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Metabolic Deficiencies in the Vitreous of Diabetic Retinopathy: Exploring the Potential of Dietary Supplementation to Address Key Metabolite Imbalances.

Metabolic Deficiencies in the Vitreous of Diabetic Retinopathy: Exploring the Potential of Dietary Supplementation to Address Key Metabolite Imbalances.

Metabolic Deficiencies in the Vitreous of Diabetic Retinopathy: Exploring the Potential of Dietary Supplementation to Address Key Metabolite Imbalances.

Metabolic Deficiencies in the Vitreous of Diabetic Retinopathy: Exploring the Potential of Dietary Supplementation to Address Key Metabolite Imbalances.

Purpose: This study aimed to investigate the metabolic alterations in the vitreous humor of patients with diabetes across different stages of diabetic retinopathy (DR) and explore potential dietary interventions to mitigate these changes.

Patients and methods: Vitreous samples were collected from 23 patients undergoing vitrectomy and grouped into controls, diabetic without DR, non-proliferative DR (NPDR), and proliferative DR (PDR). Metabolomic analysis was performed using mass spectrometry, focusing on identifying significantly altered metabolites.

Results: A total of 82 features were identified, of which several were significantly reduced in DR compared to controls. Ascorbate and taurine were notably lower in NPDR (p < 0.01), while choline and N-acetylaspartic acid were significantly reduced in NPDR and PDR (p < 0.01). Tagatose was significantly reduced in PDR (p < 0.05), while stachydrine and serine displayed biphasic trends, decreasing in NPDR (p < 0.001; p < 0.05) but increasing in PDR (p < 0.05).

Conclusion: The results suggest that key metabolites involved in antioxidant defense, membrane integrity, and neuronal function are disrupted in the vitreous humor of patients with DR. Dietary supplementation targeting these metabolic deficiencies, such as increased intake of ascorbate, taurine, serine, choline, and stachydrine, may offer adjunctive support in managing DR progression.

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