CAJ | 학술논문

目的：：观察高脂饮食诱导的胰岛素抵抗模型小鼠胰岛上胰岛素受体(IRc)/胰岛素受体底物-1(IRS-1)表达的变化。方法：20只雄性昆明小鼠随机分为高脂饲料模型组和普通饲料对照组，每组各10只。喂养20周后，观察两组小鼠大体情况，称量体重(BW)，酶法测空腹血糖(FBG)，酶联免疫法测空腹胰岛素(FIns)浓度，计算胰岛素抵抗指数(HOMA-IR)；HE 染色观察胰岛组织学变化；免疫组织化学染色分析胰岛 IRc/IRS-1的表达。比较两组各检测指标的统计学差异。结果：模型组 FBG、HOMA-IR 明显高于对照组(P 均<0.01)；胰岛边界欠完整，内部结构紊乱，伴炎性细胞浸润；IRc/IRS-1的表达较对照组明显降低(P 均<0.05)。结论：高脂饮食可成功诱导小鼠外周胰岛素抵抗，且胰岛上 IRc/IRS-1的表达降低。
목적：：관찰고지음식유도적이도소저항모형소서이도상이도소수체(IRc)/이도소수체저물-1(IRS-1)표체적변화。방법：20지웅성곤명소서수궤분위고지사료모형조화보통사료대조조，매조각10지。위양20주후，관찰량조소서대체정황，칭량체중(BW)，매법측공복혈당(FBG)，매련면역법측공복이도소(FIns)농도，계산이도소저항지수(HOMA-IR)；HE 염색관찰이도조직학변화；면역조직화학염색분석이도 IRc/IRS-1적표체。비교량조각검측지표적통계학차이。결과：모형조 FBG、HOMA-IR 명현고우대조조(P 균<0.01)；이도변계흠완정，내부결구문란，반염성세포침윤；IRc/IRS-1적표체교대조조명현강저(P 균<0.05)。결론：고지음식가성공유도소서외주이도소저항，차이도상 IRc/IRS-1적표체강저。
Objective:To observe high-fat diet induced insulin resistance mice model and the expression of islet insulin receptor(IRc)/insulin receptor substrate-1 (IRS-1).Method:20 male KM mice were randomly divided into two groups,which were fed with normal diet (control group)and high-fat diet (model group)respectively.Feeding 20 weeks later,the weight,fasting blood glucose,serum insulin levels and HOMA-IR were detected and the pancre-atic tissue was observed through tissue slice with HE.Immunohistochemical staining was used to detect the expres-sion of IRc and IRS-1.Results:The fasting blood glucose and HOMA-IR were significantly higher in model group than control group(P <0.01).Islet area was significantly less in model group than control group(P <0.05),and is-let boundary was incomplete,internal structure of islet disorder,with inflammatory cells infiltration.The expression of the IRc and IRS-1 significant decreased in model group(P <0.05).Conclusion:High-fat diet can induce insulin re-sistance of mice and decrease the expression of islet IRc/IRS-1.