世界中医药
世界中醫藥
세계중의약
WORLD CHINESE MEDICINE
2014年
6期
774-777,780
,共5页
胡照娟%张先慧%张艳红%张冬梅%娄利霞%柳红芳
鬍照娟%張先慧%張豔紅%張鼕梅%婁利霞%柳紅芳
호조연%장선혜%장염홍%장동매%루리하%류홍방
辛开苦降方%2型糖尿病%KKAy小鼠%胰岛素敏感性%糖脂代谢
辛開苦降方%2型糖尿病%KKAy小鼠%胰島素敏感性%糖脂代謝
신개고강방%2형당뇨병%KKAy소서%이도소민감성%당지대사
XinkaiKujiang formula%Type 2 diabetes mellitus%KKAy mice%Insulin sensitivity%Glucolipid metabolism
目的：观察辛开苦降方干预初发2型糖尿病（T2DM）KKAy小鼠胰岛素敏感性及糖脂代谢的影响。方法：10周龄雄性初发T2 DM KKAy小鼠40只按血糖值随机分为4组：模型组、罗格列酮组、辛开苦降低剂量组、辛开苦降高剂量组。正常对照组选10周龄雄性C57BL/6J小鼠10只。正常组及模型组给予0.5％羧甲基纤维素钠溶液（CMC）灌胃。各组连续灌胃给药四周后取材，测定其空腹血糖（Fasting Plasma glucose，FPG）、血清胰岛素（Fasting Insulin，FINS）、血脂，肝糖原、肝脂质含量。显微镜下观察肝脏组织形态。结果：给药四周后，与正常组相比，模型组胰岛素敏感指数（Insulin Sensitivity Index，ISI）明显降低（P＜0.01）， FPG、FINS、总胆固醇（Total Cholesterol，TC）、三酰甘油（Triglyceride，TG）、游离脂肪酸（Free Fatty Acid，FFA）、肝脏TC、肝脏TG均明显升高（P＜0.01），肝糖原含量降低（P＜0.01）。与模型组相比，罗格列酮组ISI好转（P＜0.01），FPG、FINS、TC、TG、FFA、TG明显降低（P＜0.01，P＜0.05），肝糖原含量明显增加（P＜0.01）。辛开苦降低剂量组及其高剂量组2组FINS、ISI、肝糖原含量均高于模型组（P＜0.05，P＜0.01），TG水平低于模型组（P＜0.05，P＜0.01）；辛开苦降高剂量还能显著降低FPG、TC水平、FFA水平（P＜0.05，P＜0.01）。辛开苦降低剂量组还可显著降低肝脏TG水平（P＜0.05）。肝脏病理显示：正常组小鼠肝脏结构正常，而模型组小鼠肝脏脂肪变性明显。罗格列酮组小鼠肝脏脂肪变性较模型组有所减轻。辛开苦降低剂量组和辛开苦降高剂量组小鼠肝脂肪变性较模型组有明显改善。结论：辛开苦降方可增加KKAy T2 DM小鼠胰岛素敏感性，减轻肝胰岛素抵抗，肝糖原合成增加，从而改善血糖水平，并能降低血及肝脏脂质水平，减轻肝脏脂肪变性，有效保护肝脏组织形态结构。
目的：觀察辛開苦降方榦預初髮2型糖尿病（T2DM）KKAy小鼠胰島素敏感性及糖脂代謝的影響。方法：10週齡雄性初髮T2 DM KKAy小鼠40隻按血糖值隨機分為4組：模型組、囉格列酮組、辛開苦降低劑量組、辛開苦降高劑量組。正常對照組選10週齡雄性C57BL/6J小鼠10隻。正常組及模型組給予0.5％羧甲基纖維素鈉溶液（CMC）灌胃。各組連續灌胃給藥四週後取材，測定其空腹血糖（Fasting Plasma glucose，FPG）、血清胰島素（Fasting Insulin，FINS）、血脂，肝糖原、肝脂質含量。顯微鏡下觀察肝髒組織形態。結果：給藥四週後，與正常組相比，模型組胰島素敏感指數（Insulin Sensitivity Index，ISI）明顯降低（P＜0.01）， FPG、FINS、總膽固醇（Total Cholesterol，TC）、三酰甘油（Triglyceride，TG）、遊離脂肪痠（Free Fatty Acid，FFA）、肝髒TC、肝髒TG均明顯升高（P＜0.01），肝糖原含量降低（P＜0.01）。與模型組相比，囉格列酮組ISI好轉（P＜0.01），FPG、FINS、TC、TG、FFA、TG明顯降低（P＜0.01，P＜0.05），肝糖原含量明顯增加（P＜0.01）。辛開苦降低劑量組及其高劑量組2組FINS、ISI、肝糖原含量均高于模型組（P＜0.05，P＜0.01），TG水平低于模型組（P＜0.05，P＜0.01）；辛開苦降高劑量還能顯著降低FPG、TC水平、FFA水平（P＜0.05，P＜0.01）。辛開苦降低劑量組還可顯著降低肝髒TG水平（P＜0.05）。肝髒病理顯示：正常組小鼠肝髒結構正常，而模型組小鼠肝髒脂肪變性明顯。囉格列酮組小鼠肝髒脂肪變性較模型組有所減輕。辛開苦降低劑量組和辛開苦降高劑量組小鼠肝脂肪變性較模型組有明顯改善。結論：辛開苦降方可增加KKAy T2 DM小鼠胰島素敏感性，減輕肝胰島素牴抗，肝糖原閤成增加，從而改善血糖水平，併能降低血及肝髒脂質水平，減輕肝髒脂肪變性，有效保護肝髒組織形態結構。
목적：관찰신개고강방간예초발2형당뇨병（T2DM）KKAy소서이도소민감성급당지대사적영향。방법：10주령웅성초발T2 DM KKAy소서40지안혈당치수궤분위4조：모형조、라격렬동조、신개고강저제량조、신개고강고제량조。정상대조조선10주령웅성C57BL/6J소서10지。정상조급모형조급여0.5％최갑기섬유소납용액（CMC）관위。각조련속관위급약사주후취재，측정기공복혈당（Fasting Plasma glucose，FPG）、혈청이도소（Fasting Insulin，FINS）、혈지，간당원、간지질함량。현미경하관찰간장조직형태。결과：급약사주후，여정상조상비，모형조이도소민감지수（Insulin Sensitivity Index，ISI）명현강저（P＜0.01）， FPG、FINS、총담고순（Total Cholesterol，TC）、삼선감유（Triglyceride，TG）、유리지방산（Free Fatty Acid，FFA）、간장TC、간장TG균명현승고（P＜0.01），간당원함량강저（P＜0.01）。여모형조상비，라격렬동조ISI호전（P＜0.01），FPG、FINS、TC、TG、FFA、TG명현강저（P＜0.01，P＜0.05），간당원함량명현증가（P＜0.01）。신개고강저제량조급기고제량조2조FINS、ISI、간당원함량균고우모형조（P＜0.05，P＜0.01），TG수평저우모형조（P＜0.05，P＜0.01）；신개고강고제량환능현저강저FPG、TC수평、FFA수평（P＜0.05，P＜0.01）。신개고강저제량조환가현저강저간장TG수평（P＜0.05）。간장병리현시：정상조소서간장결구정상，이모형조소서간장지방변성명현。라격렬동조소서간장지방변성교모형조유소감경。신개고강저제량조화신개고강고제량조소서간지방변성교모형조유명현개선。결론：신개고강방가증가KKAy T2 DM소서이도소민감성，감경간이도소저항，간당원합성증가，종이개선혈당수평，병능강저혈급간장지질수평，감경간장지방변성，유효보호간장조직형태결구。
Objective:To observe the intervention effects of XinkaiKujiang formula on insulin sensitivity and glucolipid metabolism in KKAy mice with incipient type 2 diabetes mellitus (T2DM).Methods:KKAy mice with type 2 diabetes mellitus were randomly assigned into the following four groups according to blood glucose levels:the model group,Rosiglitazone group,XinKaiKuJiang-low dose group (XK-L),XinKaiKuJiang-high dose(XK-H)group.Ten male C57BL/6J mice (10 weeks old)served as a non-diabetic control group. The mice in the control and model groups were intragastrically administered with 0.5% sodium carboxymethyl cellulose solution.Blood and tissue samples were collected after 4 weeks of treatment.Contents of fasting plasma glucose (FPG),fasting insulin (FINS),blood lipid,hepatic glycogen and liver lipid were detected,and pathological morphology in liver was observed under the microscope.Results:After 4 weeks of treatment,compared with the normal group,the insulin sensitivity index (ISI)in the model group was apparently de-creased (P<0.01).The levels of FPG,FINS,total cholesterol (TC),triglyceride (TG),free fatty acid (FFA),liver total cholesterol and liver triglycerides were significantly increased (P<0.01).The content of hepatic glycogen was decreased (P<0.01).Compared with the model group,ISI in the Rosiglitazone group was improved(P<0.01).FPG,FINS,TC,TG,FFA,and liver total cholesterol were significantly decreased (P<0.01,P<0.05).The content of hepatic glycogen was significantly increased (P<0.01).FINS,ISI,con-tent of hepatic glycogen in the XK-L group and XK-H group were all higher than those in the model group (P<0.05,P<0.01),and the level of TG was lower than that in the model group (P<0.05,P<0.01).The levels of FPG,TC and FFA could also be decreased in XK-H group (P<0.05,P<0.01).The XK-L group also could significantly decrease the liver triglyceride level (P<0.05).According to hepatic pathology,the liver structures of mice in the normal group were normal,while the livers of mice in the model group had marked fatty degeneration.Compared with model group,there was a lighter fatty degeneration of livers in Rosiglitazone group,and fatty degenera-tion of livers was significantly improved in the XK-L group and XK-H group.Conclusion:The XinkaiKujiang formula could enhance the insulin sensitivity in KKAy mice with T2DM,reduce hepatic insulin resistance,and increase the content of hepatic glycogen,further im-prove blood sugar levels.It also could lower the lipid level in blood and liver,reduce fatty degeneration of livers,and protect the morpho-logical structure of liver tissues effectively.
