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糖尿病患者的血脂糖化和脂质氧化增强。

Augmentation of blood lipid glycation and lipid oxidation in diabetic patients.

出版信息

Clin Chem Lab Med. 2014 Jan 1;52(1):47-52. doi: 10.1515/cclm-2012-0886.

DOI:10.1515/cclm-2012-0886
PMID:23454716
Abstract

Lipid oxidation plays a role in the pathophysiology of several diseases, including diabetes. Patients with type 2 diabetes show abnormally high plasma levels of phosphatidylcholine hydroperoxide (PCOOH). However, little is known about the biochemical processes that increase plasma PCOOH in diabetes. We hypothesized that "glycated lipid moieties" may form in diabetic plasma and cause oxidative stress resulting in PCOOH formation. To evaluate this hypothesis, liquid chromatography-tandem mass spectrometry (LC-MS/MS) methods were developed to analyze Amadori-glycated phosphatidylethanolamine (Amadori-PE, an early stage Maillard product), as well as the advanced glycation end products (AGE) carboxymethyl-PE (CM-PE) and carboxyethyl-PE (CE-PE). The product ion scan, neutral loss scanning, and multiple reaction monitoring provide useful structural and quantitative information about Amadori-PE, CM-PE, and CE-PE in diabetic plasma and erythrocytes. We found that plasma and erythrocyte Amadori-PE concentrations were significantly higher in diabetic patients (757±377 nM plasma, 2793±989 nM packed cells) than in normal subjects (165±66 nM plasma, 712±52 nM packed cells), and that Amadori-PE concentrations were positively correlated with PCOOH. By contrast, no significant differences were observed in blood AGE-PE concentrations between diabetic patients (CM-PE: 7.7±3.5 nM plasma, 528±83 nM packed cells; CE-PE: 2.5±1.1 nM plasma, 82±24 nM packed cells) and normal subjects (CM-PE: 6.6±3.1 nM plasma, 705±533 nM packed cells; CE-PE: 4.2±1.5 nM plasma, 68±16 nM packed cells). These results suggest that Amadori-PE is more prone to accumulation in the blood with diabetes than CM-PE or CE-PE. This review describes the involvement of blood lipid glycation and lipid oxidation in the development of diabetes.

摘要

脂质氧化在多种疾病的病理生理学中发挥作用,包括糖尿病。2 型糖尿病患者的血浆中磷脂过氧化氢(PCOOH)水平异常升高。然而,关于增加糖尿病患者血浆中 PCOOH 的生化过程知之甚少。我们假设“糖化脂质部分”可能在糖尿病患者的血浆中形成,并导致氧化应激,从而导致 PCOOH 的形成。为了评估这一假设,我们开发了液相色谱-串联质谱(LC-MS/MS)方法来分析酰基化乙醇胺(Amadori-PE,早期美拉德产物)以及晚期糖基化终产物(AGE)羧甲基-PE(CM-PE)和羧乙基-PE(CE-PE)。产物离子扫描、中性丢失扫描和多重反应监测为糖尿病患者血浆和红细胞中的 Amadori-PE、CM-PE 和 CE-PE 提供了有用的结构和定量信息。我们发现,糖尿病患者的血浆和红细胞 Amadori-PE 浓度明显高于正常受试者(血浆 757±377 nM,红细胞 2793±989 nM),且与 PCOOH 呈正相关。相比之下,糖尿病患者的血液 AGE-PE 浓度与正常受试者相比没有显著差异(CM-PE:血浆 7.7±3.5 nM,红细胞 528±83 nM;CE-PE:血浆 2.5±1.1 nM,红细胞 82±24 nM)。这些结果表明,与 CM-PE 或 CE-PE 相比,Amadori-PE 更易在糖尿病患者的血液中积累。本综述描述了血液脂质糖化和脂质氧化在糖尿病发展中的作用。

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