增殖期糖尿病视网膜病变病人不同样本代谢组学分析

    Metabolomic analysis of different samples from patients with proliferative diabetic retinopathy

    • 摘要:
      目的: 采用非靶向液相色谱–质谱联用代谢组学技术,探析增殖性糖尿期视网膜病变(PDR)病人血浆和粪便中的特征代谢物及其相关的代谢通路。
      方法: 收集蚌埠医科大学第一附属医院眼科收治的20例PDR合并玻璃体积血病人(PDR组),另择同期性别、年龄相匹配的老年性白内障住院病人20例(NDR组)。采用非靶向液相色谱–质谱技术,分别对受试者血浆和粪便代谢物进行检测。
      结果: 烟酰胺、草酸、3–亚磺酰基丙酮酸、苯乙酸在PDR组血浆和粪便中均显著升高,3, 4–二羟基苯基二醇和苯乙酰谷氨酰胺在PDR组血浆和粪便中均显著降低。基于京都基因与基因组百科全书分析显示PDR病人的血和粪标本中共同代谢通路为烟酸和烟酰胺代谢、赖氨酸降解通路、苯丙氨酸代谢、酪氨酸代谢、花生四烯酸代谢。
      结论: 烟酰胺、草酸、3–亚磺酰基丙酮酸、苯乙酸可能是PDR的致病性生物标志物,3, 4–二羟基苯基二醇、苯乙酰谷氨酰胺可能是PDR的保护性代谢物,其潜在机制可能与花生四烯酸代谢、烟酸和烟酰胺代谢、赖氨酸降解、苯丙氨酸及酪氨酸代谢等多条通路紊乱有关,这些紊乱共同促进了PDR的进展。

       

      Abstract:
      Objective To explore the characteristic metabolites and related metabolic pathways in plasma and feces of patients with proliferative diabetic retinopathy (PDR) using untargeted liquid chromatography-mass spectrometry (LC-MS)-based metabolomics.
      Methods Twenty patients with PDR complicated with vitreous hemorrhage admitted to the Department of Ophthalmology at the First Affiliated Hospital of Bengbu Medical University were enrolled as the PDR group. Another 20 sex-and-age-matched inpatients with senile cataract during the same period were selected as the NDR group. Untargeted LC-MS was applied to detect metabolites in plasma and fecal samples from the participants.
      Results Nicotinamide, oxalic acid, 3-sulfinylpyruvic acid and phenylacetic acid were significantly elevated in both plasma and feces of the PDR group, while 3,4-dihydroxyphenylethanediol and phenylacetylglutamine were significantly decreased in both plasma and feces of the PDR group. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the common metabolic pathways in plasma and fecal specimens from patients with PDR included nicotinate and nicotinamide metabolism, lysine degradation, phenylalanine metabolism, tyrosine metabolism, and arachidonic acid metabolism.
      Conclusions Nicotinamide, oxalic acid, 3-sulfinylpyruvic acid and phenylacetic acid may serve as pathogenic biomarkers of PDR, whereas 3,4-dihydroxyphenylethanediol and phenylacetylglutamine may represent protective metabolites. The underlying mechanism may be associated with disorders of multiple metabolic pathways including arachidonic acid metabolism, nicotinate and nicotinamide metabolism, lysine degradation, phenylalanine metabolism and tyrosine metabolism, which collectively contribute to the progression of PDR.

       

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