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2型糖尿病视网膜病变患者的血浆阿片肽和不对称二甲基精氨酸水平

Plasma apelin and asymmetric dimethylarginine levels in type 2 diabetic patients with diabetic retinopathy.

作者信息

Yonem Arif, Duran Cevdet, Unal Melih, Ipcioglu Osman Metin, Ozcan Omer

机构信息

Division of Endocrinology, GATA Haydarpasa Training Hospital, Istanbul, Turkey.

出版信息

Diabetes Res Clin Pract. 2009 Jun;84(3):219-23. doi: 10.1016/j.diabres.2009.03.001. Epub 2009 Apr 2.

Abstract

Oxidative stress is thought to be one of the underlying mechanisms of diabetic microvascular complications such as diabetic nephropathy and diabetic retinopathy (DRP). Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide (NO) synthase inhibitor and increased by oxidative stress. Apelin is an endogenous ligand for human orphan G-protein-coupled receptor, APJ and increases NO generation. In this study, our aim was to evaluate ADMA and apelin levels in diabetic patients with or without retinopathy and their relationships between retinopathy stages and metabolic parameters. Seventy-nine diabetic patients were included into the study and classified into three groups. Group 1 consisted of 41 patients with no DRP (NDRP), group 2 consisted of 23 patients with nonproliferative DRP (NPDRP), and group 3 consisted of 15 patients with proliferative DRP (PDRP). Plasma ADMA and apelin levels were found to be similar in all groups. But, there was a positive correlation between apelin levels and urinary albumin/creatinine ratio. Further studies involving larger patients populations and healthy controls should be done to clarify the pathogenetic significance of ADMA and apelin in diabetic microvascular complications.

摘要

氧化应激被认为是糖尿病微血管并发症(如糖尿病肾病和糖尿病视网膜病变(DRP))的潜在机制之一。不对称二甲基精氨酸(ADMA)是一种内源性一氧化氮(NO)合酶抑制剂,会因氧化应激而增加。Apelin是人类孤儿G蛋白偶联受体APJ的内源性配体,可增加NO的生成。在本研究中,我们的目的是评估患有或未患有视网膜病变的糖尿病患者的ADMA和Apelin水平,以及它们与视网膜病变阶段和代谢参数之间的关系。79名糖尿病患者被纳入研究并分为三组。第1组由41名无DRP(NDRP)的患者组成,第2组由23名非增殖性DRP(NPDRP)的患者组成,第3组由15名增殖性DRP(PDRP)的患者组成。发现所有组的血浆ADMA和Apelin水平相似。但是,Apelin水平与尿白蛋白/肌酐比值之间存在正相关。应该进行涉及更大患者群体和健康对照的进一步研究,以阐明ADMA和Apelin在糖尿病微血管并发症中的发病机制意义。

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