中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2008年
5期
537-541
,共5页
目的 探讨大黄酸改善高脂喂养联合链脲佐菌素(STZ)诱导糖尿病大鼠血糖及肝脏胰岛素敏感性的作用及其可能机制.方法 (1)55只雄性Wistar大鼠随机分为正常对照组(NC,n=15)和糖尿病组(DM,n=40).NC组以基础饲料喂养,DM组以高脂饲料喂养5周后给予一次性腹腔注射STZ(30ms/kg),其中30只成模大鼠再分为糖尿病模型组(DM-C)和糖尿病大黄酸治疗组(DM-T),后者即开始大黄酸灌胃(100 mg·kg-1·d-1),灌胃11周后处死动物,收集标本,记录体重、肝重,测定空腹血糖(FBG)、甘油三酯(TG)、总胆同醇(TC)、HbA1C、糖化血清蛋白(GSP)等生化指标,放射免疫法测定血清胰岛素浓度(FINS),计算胰岛素敏感指数(ISI)及稳态模型评估的胰岛素抵抗指数(HOMA-IR).(2)免疫组化法检测肝脏组织中PPARγ的表达,Western印迹法检测肝脏组织中葡萄糖转运蛋白2(GLUT-2)表达.结果 实验结束时,测得DM-C组FBG[(22.57±3.23 vs 7.11±1.44)mmoL/L,P<0.01]、TG[(0.89±0.29 vs 0.58±0.17)mmoL/L,P<0.01]、HbA1C[(12.49±1.96 138 8.36±0.84)%,P<0.01]、GSP[(57.29±4.14 vs13.43±2.70)μmol/L,P<0.01]和肿瘤坏死因子α[TNF-α,(1.365±0.133 vs 1.233±0.159)μg/L,P<0.05]较NC组均显著升高.DM-C组肝重指数亦明显高于NC组(0.032±0.004 vs 0.024±0.002,P<0.01),FINS与NC组无明显差别,ISI较NC组下降明显[In(ISI),-5.46±0.61 vs -4.81±0.75,P<0.05],HOMA-IR较NC组升高[In(HOMA-IR),2.34±0.64 vs 1.70±0.78,P<0.05].DM-C组肝脏PPARγ [11 131.7(5 723.1-18 979.4) vs 48 782.1(21 576.7-108 829.5),P<0.01]和GLUT-2(0.98±0.35vs 1.29±0.27,P<0.05)表达较NC组有明显下降趋势.而DM-T组大鼠的FBG[(15.94±3.16)mmol/L]、HbA1C[(10.51±1.74)%]和GSP[(47.31±6.09)μmol/L]、In(HOMA-IR)(1.86±0.30)等较DM-C组均显著降低(P<0.05或P<0.01),In(ISI)(-4.97±0.29)较DM-C组升高明显(P<0.05).肝脏PPARγ/[35 156.3(24 554.3-86 660.9)],GLUT-2(1.55±0.55)蛋白表达水平较DM-C组明显增强(P<0.05或P<0.01).结论 大黄酸可降低糖尿病大鼠血糖、HbA1C及GSP、改善糖尿病大鼠胰岛素敏感性,其机制可能与增强PPARγ、GLUT-2蛋白表达有关.
目的 探討大黃痠改善高脂餵養聯閤鏈脲佐菌素(STZ)誘導糖尿病大鼠血糖及肝髒胰島素敏感性的作用及其可能機製.方法 (1)55隻雄性Wistar大鼠隨機分為正常對照組(NC,n=15)和糖尿病組(DM,n=40).NC組以基礎飼料餵養,DM組以高脂飼料餵養5週後給予一次性腹腔註射STZ(30ms/kg),其中30隻成模大鼠再分為糖尿病模型組(DM-C)和糖尿病大黃痠治療組(DM-T),後者即開始大黃痠灌胃(100 mg·kg-1·d-1),灌胃11週後處死動物,收集標本,記錄體重、肝重,測定空腹血糖(FBG)、甘油三酯(TG)、總膽同醇(TC)、HbA1C、糖化血清蛋白(GSP)等生化指標,放射免疫法測定血清胰島素濃度(FINS),計算胰島素敏感指數(ISI)及穩態模型評估的胰島素牴抗指數(HOMA-IR).(2)免疫組化法檢測肝髒組織中PPARγ的錶達,Western印跡法檢測肝髒組織中葡萄糖轉運蛋白2(GLUT-2)錶達.結果 實驗結束時,測得DM-C組FBG[(22.57±3.23 vs 7.11±1.44)mmoL/L,P<0.01]、TG[(0.89±0.29 vs 0.58±0.17)mmoL/L,P<0.01]、HbA1C[(12.49±1.96 138 8.36±0.84)%,P<0.01]、GSP[(57.29±4.14 vs13.43±2.70)μmol/L,P<0.01]和腫瘤壞死因子α[TNF-α,(1.365±0.133 vs 1.233±0.159)μg/L,P<0.05]較NC組均顯著升高.DM-C組肝重指數亦明顯高于NC組(0.032±0.004 vs 0.024±0.002,P<0.01),FINS與NC組無明顯差彆,ISI較NC組下降明顯[In(ISI),-5.46±0.61 vs -4.81±0.75,P<0.05],HOMA-IR較NC組升高[In(HOMA-IR),2.34±0.64 vs 1.70±0.78,P<0.05].DM-C組肝髒PPARγ [11 131.7(5 723.1-18 979.4) vs 48 782.1(21 576.7-108 829.5),P<0.01]和GLUT-2(0.98±0.35vs 1.29±0.27,P<0.05)錶達較NC組有明顯下降趨勢.而DM-T組大鼠的FBG[(15.94±3.16)mmol/L]、HbA1C[(10.51±1.74)%]和GSP[(47.31±6.09)μmol/L]、In(HOMA-IR)(1.86±0.30)等較DM-C組均顯著降低(P<0.05或P<0.01),In(ISI)(-4.97±0.29)較DM-C組升高明顯(P<0.05).肝髒PPARγ/[35 156.3(24 554.3-86 660.9)],GLUT-2(1.55±0.55)蛋白錶達水平較DM-C組明顯增彊(P<0.05或P<0.01).結論 大黃痠可降低糖尿病大鼠血糖、HbA1C及GSP、改善糖尿病大鼠胰島素敏感性,其機製可能與增彊PPARγ、GLUT-2蛋白錶達有關.
목적 탐토대황산개선고지위양연합련뇨좌균소(STZ)유도당뇨병대서혈당급간장이도소민감성적작용급기가능궤제.방법 (1)55지웅성Wistar대서수궤분위정상대조조(NC,n=15)화당뇨병조(DM,n=40).NC조이기출사료위양,DM조이고지사료위양5주후급여일차성복강주사STZ(30ms/kg),기중30지성모대서재분위당뇨병모형조(DM-C)화당뇨병대황산치료조(DM-T),후자즉개시대황산관위(100 mg·kg-1·d-1),관위11주후처사동물,수집표본,기록체중、간중,측정공복혈당(FBG)、감유삼지(TG)、총담동순(TC)、HbA1C、당화혈청단백(GSP)등생화지표,방사면역법측정혈청이도소농도(FINS),계산이도소민감지수(ISI)급은태모형평고적이도소저항지수(HOMA-IR).(2)면역조화법검측간장조직중PPARγ적표체,Western인적법검측간장조직중포도당전운단백2(GLUT-2)표체.결과 실험결속시,측득DM-C조FBG[(22.57±3.23 vs 7.11±1.44)mmoL/L,P<0.01]、TG[(0.89±0.29 vs 0.58±0.17)mmoL/L,P<0.01]、HbA1C[(12.49±1.96 138 8.36±0.84)%,P<0.01]、GSP[(57.29±4.14 vs13.43±2.70)μmol/L,P<0.01]화종류배사인자α[TNF-α,(1.365±0.133 vs 1.233±0.159)μg/L,P<0.05]교NC조균현저승고.DM-C조간중지수역명현고우NC조(0.032±0.004 vs 0.024±0.002,P<0.01),FINS여NC조무명현차별,ISI교NC조하강명현[In(ISI),-5.46±0.61 vs -4.81±0.75,P<0.05],HOMA-IR교NC조승고[In(HOMA-IR),2.34±0.64 vs 1.70±0.78,P<0.05].DM-C조간장PPARγ [11 131.7(5 723.1-18 979.4) vs 48 782.1(21 576.7-108 829.5),P<0.01]화GLUT-2(0.98±0.35vs 1.29±0.27,P<0.05)표체교NC조유명현하강추세.이DM-T조대서적FBG[(15.94±3.16)mmol/L]、HbA1C[(10.51±1.74)%]화GSP[(47.31±6.09)μmol/L]、In(HOMA-IR)(1.86±0.30)등교DM-C조균현저강저(P<0.05혹P<0.01),In(ISI)(-4.97±0.29)교DM-C조승고명현(P<0.05).간장PPARγ/[35 156.3(24 554.3-86 660.9)],GLUT-2(1.55±0.55)단백표체수평교DM-C조명현증강(P<0.05혹P<0.01).결론 대황산가강저당뇨병대서혈당、HbA1C급GSP、개선당뇨병대서이도소민감성,기궤제가능여증강PPARγ、GLUT-2단백표체유관.
Objective To investigate the effects of rhein on insulin sensitivity of diabetic rats induced by high fat feeding and low dose streptozotocin (STZ), and the possible mechanisms. Methods (1) Fifty-five Wistar rats were randomly divided into normal control group (NC,n=15) and diabetes group (DM, n=40). The NC rats were fed with regular chow and DM rats were fed with high fat diet. Five weeks later, the DM rats were injected with STZ 30 mg/kg once. The 30 diabetic rats were randomly divided into two subgroups, diabetic control group (DM-C) and diabetic group treated with rhein (DM-T). DM-T rats received intragastric administration of rhein and DM-C rats were given equal doses of solvent. All rats were sacrificed eleven weeks later, the blood sample was collected. The body weight, fasting blood glucose (FBG), HbA1C, triglycerides (TG), tolal cholesterol (TC), glycosylated serum protein (GSP) and Fasting insulin (FINS) concentrations were examined.The insulin sensitive index (ISI) and homeostasis model assessment for insulin resistance (HOMA-IR) werecalculated. (2) The PPART and GLUT-2 expression in hepatic tissue were detected by immunohistoehemistry and Western-blot. Results At the end of experiment the FBG [(22.57±3.23 vs 7.11±1.44) mmol/L,P<0.01],HbA1C[(12.49±1.96 vs 8.36±0.84)%, P<0.01], TG [(0.89±0.29 vs 0.58±0.17)nunoL/L,P<0.01],GSP [(57.29±4.14 vs 13.43±2.70)μmoL/L, P<0.01] and tumor necrosis factor-α [TNF-α,(1.365±0.133 vs 1.233±0.159) μg/L, P<0.05] and the liver weight index (0.032±0.004 vs 0.024±0.002, P<0.01) in DM-C rats were higher than those in NC rats. Besides, the ISI of DM-C rats decreased [In(ISI),-5.46±0.61 vs -4.81±0.75, P<0.05] and HOMA-IR elevated [In(HOMA-IR),2.34±0.64 vs 1.70±0.78,P<0.05]. The expression of PPARγ [11 131.7(5 723.1-18 979.4) vs 48 782.1(21 576.7-108 829.5), P<0.01] and GLUT-2 (0.98±0.35 vs 1.29±0.27, P<0.05) of DM-C rats decreased markedly compared with NC rats. Compared with DM-C rats, FBG [(15.94±3.16) mmol/L], HbA1C[(10.51±1.74)%], GSP[(47-31±6.09) μmol/L] in DM-T and the In (HOMA-IR), (1.86±0.30) rats decreased (P<0.05 or P<0.01), and In (ISI), of DM-T rats increased (-4.97±0.29, P<0.05). The expressions of PPARγ [35 156.3(24 554.3-86 660.9)] and GLUT-2 (1.55±0.55) of DM-T rats were up-regulated markedly compared with DM-C rats (P<0.05 or P<0.01). Conclusion Rhein decreased FBG, HbA1C and GSP, and improved the insulin sensitivity in diabetic rats, which might be related to the up-regulated expressions of PPARγ and GLUT-2 in hepatic tissue.
