期刊文献+

急性腹腔感染与胰岛素抵抗关系及炎症因子作用时间“窗”

The relationship between acute peritoneal infection with insulin resistance and the action window time of inflammatory factors
原文传递
导出
摘要 目的探讨急性腹腔感染大鼠早期葡萄糖代谢与炎症因子水平的关系。方法SD大鼠随机分为4组:A组,盲肠结扎穿孔(CLP)组;B组,腹腔脂多糖(LPS)注射组;C组,CLP加LPS注射组;D组,对照组。A,B,C组均为急性腹腔感染模型。检测各组血浆中不同时间点葡萄糖、胰岛素、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)的水平。HOMA法计算胰岛素抵抗指数(IRI),以此评价胰岛素抵抗(IR)程度。结果大鼠急性腹腔感染组(A、B、C组)早期血浆中葡萄糖水平及IRI升高,6 h达峰值。IRI变化与TNF-α,IL-6水平的对数值之间呈正相关(r=0.609和0.755)。接受LPS注射者(B、C组)IL-6升高较未接受LPS注射组(A组)升高明显。IL-6较TNF-α维持时间延长。结论急性腹腔感染早期可出现IR;TNF-α和IL-6与IR的程度呈正相关,不同感染模型的炎症因子水平变化存在差异,其作用时间"窗"不同。 Objective To study the correlation of early glucose metabolism and inflammatory factors in rats with acute peritoneal infection. Methods Rats were randomly divided into 4 groups : A group, rats subjected to cecal ligation plus puncture ( CLP ) ; B group, to intraperitoneal injection of lipopolysaccharide ( LPS ) ; C group, to CLP combined with intraperitoneal injection of LPS C;D group, control group. A, B, C group all were to produce acute peritoneal infection. The blood glucose, TNF-α and IL-6 and insulin were detected, and insulin resistance index ( IRI ) was calculated to evaluate the extent of insulin resistance. Results Blood glucose level and IRI were elevated in the early stage in A, B, C groups, and reached a peak level at 6 h. IRI changes in the early stage had a positive correlation with TNF-α and IL-6. The rats that received LPS injection presented ( B, C groups ) mainly had a higher level of IL-6. And 1 L-6 evaluated persisted longer than TNF-α did. Conclusions Our results suggest that insulin resistance can occur in the early stage of acute peritoneal infection. Although differences exist in their action time, both TNF-α and IL-6 have a positive relationship with insulin resistance.
出处 《中国普通外科杂志》 CAS CSCD 北大核心 2009年第3期251-254,共4页 China Journal of General Surgery
基金 陕西省科技攻关项目基金(06MA208)
关键词 感染 胰岛素抵抗 肿瘤坏死因子Α 白细胞介素6 Infection Insulin Resistance Tumor Necrosis Factor-α Interleukin-6
  • 相关文献

参考文献14

  • 1Krinsley JS. Association between hypcrglyeemia and increased hospital mortality in a heterogeneous population of critically ill patients[ J]. Mayo Clin Proc,2003,78 (12) : 1471 - 1478.
  • 2Jeschke MG, Rensing H, Klein D, et al. Insulin prevents liver damage and preserves liver function in lipopolysaccharideinduced endotoxemic rats [ J ] . J Hepatol, 2005 , 42 ( 6 ) : 870 -879.
  • 3吴彪,王春友.TNF,IL-6在急性胰腺炎发病中的作用[J].中国普通外科杂志,2005,14(11):828-830. 被引量:3
  • 4燕晓雯,李维勤,王晓东,黎介寿,李宁.骨骼肌胰岛素受体底物-1及其丝氨酸磷酸化与酪氨酸磷酸化在感染大鼠胰岛素抵抗中的作用[J].中华医学杂志,2006,86(41):2922-2927. 被引量:5
  • 5Aguirre V, Werner ED, Giraud J, et al. Phosphorylation of Ser3 0 7 in insulin receptor substrate- 1 blocks interactions with the insulin receptor and inhibits insulin action [ J ]. J Biol Chem,2002,277(2) :1531 -1537.
  • 6Tremblay F, Gagnon A, Veilleux A, et al. Activation of the mammalian target of rapamycin pathway acutely inhibits insulin signaling to Akt and glucose transport in 3T3-L1 and human adipocytes [ J ] . Endocrinolgy, 2005 , 146 ( 3 ) : 1328 - 1337.
  • 7Li L, Yang G, Shi S, et al. The adipose triglyceride lipase, adiponectin and visfatin are downregulated by tumor necrosis factor-alpha ( TNF-alpha ) in vivo [ J ]. Cytokine, 2009,45 (1):9-12.
  • 8Rotter V, Nagaev I, Smith U. Interleukin-6 ( IL-6 ) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, over expression in human fat cells from insulin resistant subjects [ J ]. J Boil Chem ,2003 , 278(46) :45777 -45784.
  • 9Kim JH, Kim JE, Liu HY, et al. Regulation of IL-6 induced hepatic insulin resistance by rotor through the stat3-socs3 pathway[J]. J Biol Chem,2008,283(2) :708 -715.
  • 10Andreozzi F, Laratta E, Procopio C, et al. Interleukin-6 impairs the insulin signaling pathway, promoting production of nitric oxide in human umbilical vein endothelial ceils [ J ]. Mol Cell Biol,2007,27(6) :2372-2383.

二级参考文献20

  • 1燕晓雯,李维勤,虞文魁,王晓东,李宁,黎介寿.外科感染病人胰岛素抵抗及其相关因素分析[J].外科理论与实践,2006,11(1):14-19. 被引量:16
  • 2Rinderknecht H. Pancreatitis, a consequence of excessive leukocyte timulation[J]. Int J pancretol,1988,3(2 ~3):105 -112.
  • 3吴爱娟.各种实验动物标本的固定、脱水、透明、浸蜡等部题的探讨[J].中华病理学杂志,1987,16(4):709-310.
  • 4Kusser AM, Rongione A J, Ashley SW, et al. In terleukin-10 prevents death in lethal necosizing pancreatitis in mice [ J ]. Surgery, 1996, 120(11): 284 -289.
  • 5Norman J, Denham W, Chapman V, et al. TNF induces acinar cell. apoptotsis during acute pancreatitis [ J ]. Gastroenterology,1999,112(9): A468.
  • 6Hsu H, Shu HB, Pan MG, et al. TRADD-TRAF2 and TRADDF ADD interactions define two distinct TNF receptor Ⅰ signal tranduction pathways [ J ]. Cell, 1999,84 ( 8 ): 299 - 308.
  • 7Carlson GL.Insulin resistance in sepsis.Br J Surg,2003,90:259-260.
  • 8Saltiel AR,Kahn CR.Insulin signaling and the regulation of glucose and lipid metabolism.Nature,2001,414:799-806.
  • 9Singleton KD,Wischmeyer PE.Distance of cecum ligated influences mortality,tumor necrosis factor-alpha and interleukin-6 expression following cecal ligation and puncture in the rat.Eur Surg Res,2003,35:486-491.
  • 10Mather KJ,Hunt AJ,Steinberg HO,et al.Repeatability characteristics of simple indices of insulin resistance:implications for research applications.J Clin Endocrinol Metab,2001,86:5457-5464.

共引文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部