浙江医学
浙江醫學
절강의학
ZHEJIANG MEDICAL JOURNAL
2013年
1期
3-5
,共3页
周华丽%徐明智%胡玲玲%陆珣靓%李成江
週華麗%徐明智%鬍玲玲%陸珣靚%李成江
주화려%서명지%호령령%륙순정%리성강
2 型糖尿病%动物模型%微血管并发症%大血管并发症
2 型糖尿病%動物模型%微血管併髮癥%大血管併髮癥
2 형당뇨병%동물모형%미혈관병발증%대혈관병발증
Type 2 diabetes%Rat model%Microvascular complications%Macrovascular complications
目的用普通大鼠,通过持续高脂饲料加单次小剂量链脲佐菌素(streptozocin,STZ)诱导,建立2型糖尿病模型目前尚待改进饲料配方.方法重约200~250g 的雄性 SD 大鼠48只,随机分成4组:普通饲料对照组和3个梯度的高脂饲料组.各高脂饲料组大鼠4 周时予 STZ 30mg/kg 单次腹腔注射.分别在3、6和12个月分批处死,进行生化检测和病理观察.结果各组糖尿病大鼠表现为腹型肥胖,空腹血糖>7.8mmol/L,不依赖胰岛素而存活,血脂谱为“高 TG、低 HDL 和高 LDL 或 TC”.持续高脂诱导3个月后,各组大鼠均出现肺、心肌、肾、大脑、骨骼肌、眼球、阴茎和膀胱等全身多脏器小动脉硬化,但主动脉弓未见明显变化.持续高脂诱导6~12个月后,脂肪含量最高的 I 号饲料喂养的大鼠出现主动脉弓内膜钙化斑,弹力纤维的扭曲、断裂.结论高脂饲料+单次小剂量 STZ 诱导,可使大鼠较短期内出现全身小动脉硬化;但对于明显动脉粥样硬化的建模,可能尚需进一步提高饲料的脂肪含量或添加血管损伤剂.
目的用普通大鼠,通過持續高脂飼料加單次小劑量鏈脲佐菌素(streptozocin,STZ)誘導,建立2型糖尿病模型目前尚待改進飼料配方.方法重約200~250g 的雄性 SD 大鼠48隻,隨機分成4組:普通飼料對照組和3箇梯度的高脂飼料組.各高脂飼料組大鼠4 週時予 STZ 30mg/kg 單次腹腔註射.分彆在3、6和12箇月分批處死,進行生化檢測和病理觀察.結果各組糖尿病大鼠錶現為腹型肥胖,空腹血糖>7.8mmol/L,不依賴胰島素而存活,血脂譜為“高 TG、低 HDL 和高 LDL 或 TC”.持續高脂誘導3箇月後,各組大鼠均齣現肺、心肌、腎、大腦、骨骼肌、眼毬、陰莖和膀胱等全身多髒器小動脈硬化,但主動脈弓未見明顯變化.持續高脂誘導6~12箇月後,脂肪含量最高的 I 號飼料餵養的大鼠齣現主動脈弓內膜鈣化斑,彈力纖維的扭麯、斷裂.結論高脂飼料+單次小劑量 STZ 誘導,可使大鼠較短期內齣現全身小動脈硬化;但對于明顯動脈粥樣硬化的建模,可能尚需進一步提高飼料的脂肪含量或添加血管損傷劑.
목적용보통대서,통과지속고지사료가단차소제량련뇨좌균소(streptozocin,STZ)유도,건립2형당뇨병모형목전상대개진사료배방.방법중약200~250g 적웅성 SD 대서48지,수궤분성4조:보통사료대조조화3개제도적고지사료조.각고지사료조대서4 주시여 STZ 30mg/kg 단차복강주사.분별재3、6화12개월분비처사,진행생화검측화병리관찰.결과각조당뇨병대서표현위복형비반,공복혈당>7.8mmol/L,불의뢰이도소이존활,혈지보위“고 TG、저 HDL 화고 LDL 혹 TC”.지속고지유도3개월후,각조대서균출현폐、심기、신、대뇌、골격기、안구、음경화방광등전신다장기소동맥경화,단주동맥궁미견명현변화.지속고지유도6~12개월후,지방함량최고적 I 호사료위양적대서출현주동맥궁내막개화반,탄력섬유적뉴곡、단렬.결론고지사료+단차소제량 STZ 유도,가사대서교단기내출현전신소동맥경화;단대우명현동맥죽양경화적건모,가능상수진일보제고사료적지방함량혹첨가혈관손상제.
Objective To establish type 2 diabetes rat model by high-fat diet and single low-dose streptozotocin. Methods Forty eight male SD rats (200-250 g) were randomly divided into 4 groups. Rats in group I-III were fed with three gra-dient high-fat diets, and rats in group IV were fed with regular chow. The rats in high-fat diet groups were given a single dose of streptozotocin (30mg/kg) intraperitoneal y. The rats were sacrificed at the end of the 3rd, 6th and 12th months (4 rats in each group). The weight, abdominal circumference and body length were measured, the blood glucose and lipid profile were exam-ined and the pathological changes were observed. Results The rats in the high-diet groups all presented abdominal obesity. The fasting blood glucose was >7.8mmol/L, and the rats survived without insulin treatment. The lipid profiles presented as high triglycerides, low HDL and high LDL or total cholesterol. When sacrificed after feeding with high-fat diet for 3 months, arteriolar sclerosis was found in the lungs, myocardium, kidneys, brain, skeletal muscles, eyebal s, penis and bladder in the rats of high-fat diet groups. When sacrificed after feeding with high-fat diets for 6-12 months, intimal calcification, twisting or broken elastic fiber were found in the aorta arch in the rats fed with the highest fat diet, but not in the other two high-fat groups. Conclusion Type 2 diabetes rat model can be established by high-fat diet and single low dosage of streptozotocin. Arteriolar sclerosis can be ob-served in multiple organs via inducing for 3 months. However, significant atherosclerosis in the aorta may require to be induced by diet consisting of more fat or supplemented with vascular damaging agents.