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内源性分泌型糖基化终产物受体与2型糖尿病颈动脉粥样硬化的关系 被引量:5

Association of endogenous secretory receptor for advanced glycation end products with carotid atherosclerosis in type 2 diabetes mellitus
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摘要 目的探讨内源性分泌型糖基化终产物受体(esRAGE)水平与2型糖尿病(T2DM)颈动脉粥样硬化的关系。方法60例T2DM患者,分成颈动脉粥样硬化组(A组,30例)和无颈动脉粥样硬化组(B组,30例)。28例非糖尿病者为对照组(C组)。分别检测esRAGE浓度、体重指数、血压、血脂和糖化血红蛋白(HbA1c)。结果A组和B组esRAGE浓度均明显低于C组(P<0.05),A组明显低于B组(P<0.01)。多危险因素与T2DM颈动脉粥样硬化Logistic回归分析表明,esRAGE是T2DM颈动脉粥样硬化的重要保护因素(b<0,OR<1,P<0.1)。结论esRAGE与T2DM密切相关,对T2DM颈动脉粥样硬化有潜在保护作用。 Objective To evaluate the association of endogenous secretory receptor for advanced glycation end products (esRAGE) with carotid atherosclerosis(CAS) in type 2 diabetes mellitus (T2DM). Methods Sixty T2DM patients were assigned into group A(with CAS) and group B(without CAS).Another 28 nondiabetic subjects were used as the normal control(group C). esRAGE,body mass index(BMI),blood pressure,lipids,glycosylated hemoglobin A1c(HbA1c) were measured.Results esRAGE was significantly lower in group A and B than that in group C (P〈0.05),which was significantly lower in group A than that in group B(P〈0.01).Logistic regression analysis showed that esRAGE was the important protective factor for CAS in T2DM (b〈0,OR〈1,P〈0.1).Conclusion esRAGE is associated with T2DM,and is a novel and potential protective factor for CAS in T2DM.
出处 《江苏医药》 CAS CSCD 北大核心 2008年第5期468-469,共2页 Jiangsu Medical Journal
关键词 内源性分泌型糖基化终产物受体 2型糖尿病 颈动脉粥样硬化 Endogenous secretory receptor for advanced glycation end products Type 2 diabetes mellitus Carotid atherosclerosis
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  • 1Yan SF, Rarnasamy R, Naka Y, et al. Glyeation, inflammation and RAGE: a scaffold for the macro-vascular complications of diabetes and beyond[J]. Cire Res, 2003,93(12) : 1159-1169.
  • 2Yonekura H, Yamamoto Y, Sakurai S, et al. Roles of the receptor for advanced glycation endproducts in diabetes induced vascular injury.[J]. J Phamacol Sci, 2005,97(3): 305-311.
  • 3Koyama H, Yokoyama H, Motoyama K, et al. Plasma level of endogenous secretory RAGE is associated with components of the metabolic syndrome and atherosclerosis[J]. Arterioscler Thromb Vasc Biol, 2005,25 (12) : 2587-2593.

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