CAJ | 학술논문

目的：探索游泳运动对大鼠胰岛Fractalkine（FKN）表达及P13K／Akt信号通路影响，进一步阐明有氧运动改善糖尿病糖代谢的机制。方法：本研究以雄性成年SD大鼠为实验对象，利用高脂高糖饲料加腹腔注射链脲佐菌素（STZ，30mg／kg）建立2型糖尿病胰岛素抵抗大鼠模型（T2DM）。按一定时间对大鼠进行游泳训练。采用血清学检测试剂盒血清中胰岛素和血糖的含量，计算大鼠的胰岛素抵抗指数（HOMAqR）。免疫印迹技术检测骨骼肌中葡萄糖转运蛋白4（GLUT4）和胰岛中FKN及P13K／Akt信号蛋白的表达。结果：与正常大鼠相比，糖尿病大鼠血清胰岛素和空腹血糖水平显著增加，HO-MA—IR升高；腓肠肌GLUT4和胰腺组织中FKN及P13K／Akt信号分子的表达降低。施加游泳训练后，T2DM大鼠腓肠肌GLUT4和胰岛中FKN的表达及P13K／Akt信号分子的表达显著增加（声〈0．05），同时，血清胰岛素和空腹血糖水平及HOMA_IR显著降低。结论：长期有氧运动明显改善T2DM血糖代谢，其机制可能与运动降低T2DM大鼠胰岛素抵抗，激活P13K／Akt信号通路促进FKN表达保护胰岛功能有关。
목적：탐색유영운동대대서이도Fractalkine（FKN）표체급P13K／Akt신호통로영향，진일보천명유양운동개선당뇨병당대사적궤제。방법：본연구이웅성성년SD대서위실험대상，이용고지고당사료가복강주사련뇨좌균소（STZ，30mg／kg）건립2형당뇨병이도소저항대서모형（T2DM）。안일정시간대대서진행유영훈련。채용혈청학검측시제합혈청중이도소화혈당적함량，계산대서적이도소저항지수（HOMAqR）。면역인적기술검측골격기중포도당전운단백4（GLUT4）화이도중FKN급P13K／Akt신호단백적표체。결과：여정상대서상비，당뇨병대서혈청이도소화공복혈당수평현저증가，HO-MA—IR승고；비장기GLUT4화이선조직중FKN급P13K／Akt신호분자적표체강저。시가유영훈련후，T2DM대서비장기GLUT4화이도중FKN적표체급P13K／Akt신호분자적표체현저증가（성〈0．05），동시，혈청이도소화공복혈당수평급HOMA_IR현저강저。결론：장기유양운동명현개선T2DM혈당대사，기궤제가능여운동강저T2DM대서이도소저항，격활P13K／Akt신호통로촉진FKN표체보호이도공능유관。
The objective of this study was to investigate the effect of exercise on the expressions of Fractalkine （FKN） and phosphatidylinositol 3 kinase （P13K0/protein kinase B （PKB, Akt） signal pathway in the pancreas of Type 2 diabetic rats （T2DM）. Adult male SD rats were used to develop the Type 2 diabetic models by the high fat and high-glucose diet, intraperitoneal injection of streptozotocin （STZ, 30 mg/kg）. The rats were trained in swimming by schedule procedures.Index of insulin resistance （HOMA-IR） was calculated respectively by values of serum insulin and fasting blood-glucose （FBG） determined by kits. Western blotting was applied to detect the protein expression of glucose transport proteins （GLUT4）, P13K/Akt and FKN. It could be seen that compared with rats in the control groups, the diabetic rats showed significantly increased levels of serum insulin and FBG, the index of insulin resistance, the protein expressions of muscle GLUT4 and PKN, phosphorylation of P13K/Akt decreased. Exercise training decreased HOMA-IR, increase the expressions of muscle GLUT4, pancreatic FKN and P13 K/Akt （P〈 0.05）. It meant that exercise training could promote the glucose metabolism. The mechanism was related to the decreased HOMA-IR and increase the expression of pancreatic FKN through P13 K/Akt.