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血清脂肪因子血管生成素样蛋白4水平与2型糖尿病下肢血管病变的相关性研究 被引量:14

Correlation between serum ANGPTL4 and lower limb angiopathy in patients with type 2 diabetes mellitus
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摘要 目的探讨T2DM患者血清脂肪因子血管生成素样蛋白4(ANGPTL4)变化及其与下肢血管病变的关系。方法选取151例T2DM患者,按是否发生下肢血管病变分为非下肢血管病变组(n=76)和下肢血管病变组(n=75),另选50名健康者为正常对照组(NC)。下肢血管病变分为A级、B级、C级。ELISA检测血清ANGPTL4水平,并分析其与其他临床指标的相关性。结果下肢血管病变组、非下肢血管病变组和NC组血清ANGPTL4水平依次升高(P<0. 01)。下肢血管病变组(B级和C级)血清ANGPTL4水平低于A级,且C级低于B级(P<0. 01)。多元逐步回归分析显示,FPG、血清白蛋白、HbA1c、TG、TC、HDL-C、LDL-C、ANGPTL4是T2DM患者下肢血管病变的影响因素。结论血清ANGPTL4水平与T2DM患者下肢血管病变相关,是T2DM下肢血管病变的潜在早期预测指标。 Objective To investigate the changes of serum level of adipokine angiopoietin-like protein 4(ANGPTL4)in patients with type 2 diabetes mellitus(T2 DM)and the relationship between ANGPTL4 and diabetic lower limb angiopathy.Methods151 T2 DM patients were selected and divided into non-lower limb vascular disease group and lower limb vascular disease group. 50 healthy patients were selected as the control group. Serum ANGPTL4 level was detected by ELISA.ResultsSerum ANGPTL4 levels in T2 DM patients were lower than those in control group(P<0. 01),especially in patients with lower limb angiopathy(P<0. 01). Serum ANGPTL4 levels showed a downward trend from grade A to B and C of aggravating lower extremity vascular lesions(P<0. 01). Multiple stepwise regression analysis showed that FPG,ALB,HbA1 c,TG,TC,HDL-C,LDL-C,ANGPTL4 were the influencing factors of lower limb vascular lesions in T2 DM patients.ConclusionSerum ANGPTL4 level is correlated with extremity vascular disease inT2 DM patients and may be a potential early predictor.
作者 胡丹丹 林霞 曾建 HU Dandan;LIN Xia;ZENG Jian(Department of Medicine,Fujian Provincial Armed Police Corps Hospital,Fuzhou 350000,China)
出处 《中国糖尿病杂志》 CAS CSCD 北大核心 2019年第6期434-437,共4页 Chinese Journal of Diabetes
关键词 脂肪因子血管生成素样蛋白4 糖尿病 2型 下肢血管病变 相关性 Adipokine angiopoietin-like protein 4 Diabetes mellitus,type 2 Lower limb angiopathy Correlation
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  • 1Koreeka A, de Wouters T, Cuhrone A, et al. ANGPTL4 ex- pression induced by butyrate and rosiglitazone in human intesti- nal epithelial cells utilizesindependent pathways. Am J Physiol Gastrointest Liver Physiol, 2013,304 .- 1025-1037.
  • 2Clement LC, Mac C, Avila Casado C, et al. Circulating angio- poietin-like 4 links proteinuria with hypertriglyeeridemia in ne- phrotic syndrome. Nat Med, 2014,20 : 37-46.
  • 3Chugh SS, Clement LC, Mac6 C. New insights into human mini- mal change disease: lessons from animal models. Am J Kidney Dis, 2012,59.. 284 292.
  • 4van Raahe DH, Brands M, Serlie MJ, et al. Angiopoietimlike protein 4 is dif{erentially regulated by glueocorticoids and insu- lin in vitro and in vivo in healthy humans. Exp Clin Endocrinol Diabetes, 2012,120 : 598-603.
  • 5Vaziri ND, Moradi H. Dual role of drculating angiopoietin-like 4 (ANGFrFIA) in promoting hypertriglyeeridemia and lowering proteinuria in nephrotic syndrome. Am Kidney Dis, 2014,64; 495-498,.
  • 6Georgiadi A, Lichtenstein L, Degenhardt T, et al. Induction of cardiac ANGPTIA by dietary fatty acids is mediated by peroxi- some proliferator-activated receptorbeta/delta and protects a- gainst fatty acid-induced oxidative stress. Circ Res, 2010, 106= 1712-1721.
  • 7Bouleti C, Mathivet T, Coqueran B, et al. Protective effects of angiopoietin-like 4 on eerebrovaseular and functional damages in ischaemie stroke. Eur Heart J, 2013,34 = 3657-3668.
  • 8Wang Y, Chen H, Li H, et al. Effect of angiopoietin-like protein 4 on rat pulmonary microvascular endothelial cells exposed to LPS. Int J Mol Med, 2013,32 = 568-576.
  • 9Gray NE, Lain LN, Yang K, et al. Angiopoietin-like 4 (ANGPTIA) protein is a physiological mediator of intracellular lipolysis in routine adipocytes J Biol Chem, 2012,287 = 8444-8456.
  • 10Kim YS, Kang H.J, Hong MH, et al. Angiopoietin - like 4 is involved in the poor angiogenic potential of high glucose - insulted bone marrow stem cells [ J ]. Korean circulation journal, 2014,44 ( 3 ) : 177-183.

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