中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2012年
1期
45-48
,共4页
庄秋林%吴国豪%蒋奕%张波%韩寓嵩
莊鞦林%吳國豪%蔣奕%張波%韓寓嵩
장추림%오국호%장혁%장파%한우숭
脂连素%创伤%胰岛素抵抗%胰岛素受体底物蛋白1%蛋白激酶B
脂連素%創傷%胰島素牴抗%胰島素受體底物蛋白1%蛋白激酶B
지련소%창상%이도소저항%이도소수체저물단백1%단백격매B
Adiponectin%Trauma%Insulin resistance%Insulin receptor substrate 1%Protein kinase B
目的 观察创伤后胰岛素抵抗现象,探讨脂连素对手术创伤导致的胰岛素抵抗的作用和机制.方法 60只SD大鼠随机分为脂连素组(n=20)、创伤组(n=20)以及对照组(n=20).建立大鼠创伤模型,脂连索组运用脂连素进行预处理(1 mg/kg腹腔内注射),测定大鼠的血糖及血清胰岛素浓度,计算胰岛素抵抗指数(HOMA-IR)和胰岛素分泌指数(HOMA-β)；检测骨骼肌胰岛素受体底物蛋白-1( IRS-1)、蛋白激酶B(PKB/Akt)的含量及其磷酸化状态.结果 创伤组与对照组比较血糖浓度明显升高(P＜0.05),血清胰岛素浓度先短暂下降然后逐渐升高(P＜0.05).HOMA-IR明显高于对照组(P＜0.05),HOMA-β则低于对照组(P＜0.05).脂连素组大鼠血糖浓度明显下降(P＜0.05),血清胰岛素浓度无明显改变(P＞0.05).HOMA-IR明显下降(P＜0.05),HOMA-β明显上升(P＜0.05).创伤组与对照组、脂连素组与创伤组大鼠骨骼肌中总的IRS-1及PKB/Akt蛋白含量无明显差异,但创伤组较对照组大鼠骨骼肌的IRS-1酪氨酸(Tyr)位点的磷酸化水平下降了31％[ (88.54±33.48)比(128.60±33.19),F=0.108,P＜0.01],丝氨酸(Ser)位点磷酸化水平增加了64％[(154.31±36.94)比(94.20±27.88),F=0.602,P＜0.01],PKB/Akt的磷酸化水平下降了46％[ (46.58±2.48)比(86.32±3.31),F=0.153,P＜0.01].脂连素组大鼠的骨骼肌IRS-1 Tyr位点的磷酸化水平较创伤组上升了23％[(109.05±30.77)比(88.54±33.48),F=0.012,P＜0.01],而Ser位点磷酸化水平下降了30％ [(118.65±33.49)比(154.31±36.94),F=0.272,P＜0.01],PKB/Akt的磷酸化水平上升了56％[ (72.73±2.95)比(46.58±2.48),F=0.473,P＜0.01].结论 大鼠创伤后存在胰岛素抵抗现象,其机制与胰岛素受体后信号转导通路受阻有关.脂连素能缓解创伤后胰岛素抵抗途径的发生和发展,从而改善创伤后胰岛索抵抗产生的高血糖.
目的 觀察創傷後胰島素牴抗現象,探討脂連素對手術創傷導緻的胰島素牴抗的作用和機製.方法 60隻SD大鼠隨機分為脂連素組(n=20)、創傷組(n=20)以及對照組(n=20).建立大鼠創傷模型,脂連索組運用脂連素進行預處理(1 mg/kg腹腔內註射),測定大鼠的血糖及血清胰島素濃度,計算胰島素牴抗指數(HOMA-IR)和胰島素分泌指數(HOMA-β)；檢測骨骼肌胰島素受體底物蛋白-1( IRS-1)、蛋白激酶B(PKB/Akt)的含量及其燐痠化狀態.結果 創傷組與對照組比較血糖濃度明顯升高(P＜0.05),血清胰島素濃度先短暫下降然後逐漸升高(P＜0.05).HOMA-IR明顯高于對照組(P＜0.05),HOMA-β則低于對照組(P＜0.05).脂連素組大鼠血糖濃度明顯下降(P＜0.05),血清胰島素濃度無明顯改變(P＞0.05).HOMA-IR明顯下降(P＜0.05),HOMA-β明顯上升(P＜0.05).創傷組與對照組、脂連素組與創傷組大鼠骨骼肌中總的IRS-1及PKB/Akt蛋白含量無明顯差異,但創傷組較對照組大鼠骨骼肌的IRS-1酪氨痠(Tyr)位點的燐痠化水平下降瞭31％[ (88.54±33.48)比(128.60±33.19),F=0.108,P＜0.01],絲氨痠(Ser)位點燐痠化水平增加瞭64％[(154.31±36.94)比(94.20±27.88),F=0.602,P＜0.01],PKB/Akt的燐痠化水平下降瞭46％[ (46.58±2.48)比(86.32±3.31),F=0.153,P＜0.01].脂連素組大鼠的骨骼肌IRS-1 Tyr位點的燐痠化水平較創傷組上升瞭23％[(109.05±30.77)比(88.54±33.48),F=0.012,P＜0.01],而Ser位點燐痠化水平下降瞭30％ [(118.65±33.49)比(154.31±36.94),F=0.272,P＜0.01],PKB/Akt的燐痠化水平上升瞭56％[ (72.73±2.95)比(46.58±2.48),F=0.473,P＜0.01].結論 大鼠創傷後存在胰島素牴抗現象,其機製與胰島素受體後信號轉導通路受阻有關.脂連素能緩解創傷後胰島素牴抗途徑的髮生和髮展,從而改善創傷後胰島索牴抗產生的高血糖.
목적 관찰창상후이도소저항현상,탐토지련소대수술창상도치적이도소저항적작용화궤제.방법 60지SD대서수궤분위지련소조(n=20)、창상조(n=20)이급대조조(n=20).건립대서창상모형,지련색조운용지련소진행예처리(1 mg/kg복강내주사),측정대서적혈당급혈청이도소농도,계산이도소저항지수(HOMA-IR)화이도소분비지수(HOMA-β)；검측골격기이도소수체저물단백-1( IRS-1)、단백격매B(PKB/Akt)적함량급기린산화상태.결과 창상조여대조조비교혈당농도명현승고(P＜0.05),혈청이도소농도선단잠하강연후축점승고(P＜0.05).HOMA-IR명현고우대조조(P＜0.05),HOMA-β칙저우대조조(P＜0.05).지련소조대서혈당농도명현하강(P＜0.05),혈청이도소농도무명현개변(P＞0.05).HOMA-IR명현하강(P＜0.05),HOMA-β명현상승(P＜0.05).창상조여대조조、지련소조여창상조대서골격기중총적IRS-1급PKB/Akt단백함량무명현차이,단창상조교대조조대서골격기적IRS-1락안산(Tyr)위점적린산화수평하강료31％[ (88.54±33.48)비(128.60±33.19),F=0.108,P＜0.01],사안산(Ser)위점린산화수평증가료64％[(154.31±36.94)비(94.20±27.88),F=0.602,P＜0.01],PKB/Akt적린산화수평하강료46％[ (46.58±2.48)비(86.32±3.31),F=0.153,P＜0.01].지련소조대서적골격기IRS-1 Tyr위점적린산화수평교창상조상승료23％[(109.05±30.77)비(88.54±33.48),F=0.012,P＜0.01],이Ser위점린산화수평하강료30％ [(118.65±33.49)비(154.31±36.94),F=0.272,P＜0.01],PKB/Akt적린산화수평상승료56％[ (72.73±2.95)비(46.58±2.48),F=0.473,P＜0.01].결론 대서창상후존재이도소저항현상,기궤제여이도소수체후신호전도통로수조유관.지련소능완해창상후이도소저항도경적발생화발전,종이개선창상후이도색저항산생적고혈당.
Objective To explore the mechanism of posttraumatic insulin resistance and confirm that adiponectin can improve posttraumatic insulin resistance in rats.Methods Sixty SD rats were divided into three groups:adiponectin group ( n =20 ),operation group ( n =20 ),and control group ( n =20 ).The surgical trauma model was established.In adiponectin group,rats were pretreated with adiponectin (1 mg/kg intraperitoneal injection).The levels of blood glucose and serum insuhn were determined.The index of insulin resistance (HOMA-IR) and the index of insulin secretion (HOMA-β) were calculated and several key proteins in the insulin signaling such as insulin receptor substrate 1 ( IRS-1 ),protein kinase B (PKB/Akt) in skeletal muscle were measured respectively.Results Compared with the control group,the level of blood glucose was elevated significantly,the level of serum insulin decreased 30 min after operation but elevated thereafter in operation group.HOMA-IR was significantly higher while the index of insulin secretion HOMA-β was lower in the operation group than in the control group.In adiponectin group the level of blood glucose was decreased significantly as compared with the the operation group,but there there was no significant difference in the level of serum insulin between the operation group and adiponectin group.HOMA-IR was significantly lower and HOMA-β was higher in the adiponectin group than in the operation group.There was no significant difference in the total content of IRS-1 and PKB/Akt in skeletal muscle between the operation and control groups or between the adiponectin and operation groups.But the phosphorylation of tyrosine (Tyr) residue of IRS-1 seen in the operation group was attenuated by 31％ [ (88.54 ± 33.48 ) vs.( 128.60 ± 33.19 ),F =0.108,P ＜ 0.01 ],whereas the phosphorylation of serine (Ser) residue of IRS-1 was significantly enhanced by 64％ [ ( 154.31 ± 36.94) vs.(94.20 ± 27.88 ),F =0.602,P ＜0.0l ] and the phosphorylation state of PKB/Akt was attenuated by 46％ compared with the control group [(46.58 ±2.48) vs.(86.32 ±3.31),F=0.153,P＜0.01].As compared with the operation group,the phosphorylation of Tyr residue of IRS-1 in the adiponectin group was enhanced by 23％ [ ( 109.05 ± 30.77) vs.(88.54 ± 33.48 ),F =0.012,P ＜ 0.01 ],whereas that of Ser residue of I RS-1 was significantly attenuated by 30％ [ ( 118.65 ± 33.49 ) vs.( 154.31 ± 36.94 ),F =0.272,P ＜ 0.01 ],and the phosphorylation state of PKB/Akt was also enhanced by 56％ [ (72.73 ± 2.95) vs.(46.58 ±2.48),F =0.473,P ＜ 0.01 ].Conclusion The surgical trauma induced posttraumatic insulin resistance,which was associated with the block of insulin signal transduction.Adiponectin can alleviate the development of insulin signal transduction pathway after surgical trauma and improve post-traumatic insuhn resistance which resulting in high blood glucose.
