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首页> 外文期刊>International Journal of Experimental Pathology >Establishment of a diabetic myocardial hypertrophy model in Mus musculus castaneus mouse
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Establishment of a diabetic myocardial hypertrophy model in Mus musculus castaneus mouse

机译:在Mus Musculus Castaneus鼠标中建立糖尿病心肌肥大模型

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摘要

The aim of this study was to establish a robust model of diabetic myocardial hypertrophy in Mus musculus castaneus mice. Mice were fed a high-fat diet for four weeks and then given streptozotocin (STZ, 40 mg kg(-1) d(-1) for 5 days, intraperitoneally) and fasting blood glucose (FBG) levels were tested after seven days. Mice with FBG levels above 11.1 mmol/L were considered diabetic. Diabetic mice continued to have access to the high-fat diet until cardiac hypertrophy developed. FBG and body weight (BW) were measured weekly. Myocardial hypertrophy was confirmed by left ventricle (LV) hypertrophy index (LVHI), LV/BW, LV histopathological observation and atrial natriuretic factor (ANF) mRNA expression. Serum insulin and plasma haemoglobin A1c (HbA1c) levels, total cholesterol (TCH) and triglyceride (TG) were measured, and then an insulin resistance index (HOMA.IR) was calculated. The level of FBG in the model group remained above 11.1 mmol/L, and the BW showed significant weight loss, compared with the control group (P0.01). The high levels of HbA1c, HOME.IR, TCH and TG, and the low level of insulin suggested that glucose metabolism was not balanced with insulin resistance; meanwhile, higher TCH and TG showed that dyslipidaemia had also developed. After the diabetic mice were kept on the high-energy diet for another four weeks, histopathological observation showed myocardial injuries, much more surface area and collagen fibres, higher LVHI and LV/BW, and elevated expression of ANF mRNA (P0.01), suggesting that myocardial hypertrophy had appeared in Mus musculus castaneus mice under the current experimental conditions. Thus a robust model of diabetic myocardial hypertrophy was established four weeks after confirmation of diabetes, which was induced by feeding a high-fat diet for four weeks combined with a repeated low-dose STZ exposure, in Mus musculus castaneus mice.
机译:本研究的目的是在Mus Musculus Castaneus小鼠中建立一种稳健的糖尿病心肌肥厚模型。将小鼠喂养高脂饮食四周,然后给予链脲佐菌素(STZ,40mg kg(-1)d(-1)5天,腹膜内)和腹腔葡萄糖(FBG)水平在七天后进行测试。具有11.1mmol / L以上的FBG水平的小鼠被认为是糖尿病。直到心脏肥大的发展,糖尿病小鼠继续获得高脂肪饮食。每周测量FBG和体重(BW)。通过左心室(LV)肥大指数(LVHI),LV / BW,LV组织病理学观察和心房Natriuric因子(ANF)mRNA表达来证实心肌肥大。测定血清胰岛素和血浆血红蛋白A1C(HBA1C)水平,总胆固醇(TCH)和甘油三酯(TG),然后计算胰岛素抗性指数(HOMA.IR)。模型组中的FBG水平仍然高于11.1mmol / L,与对照组相比,BW显示出显着的体重减轻(P <0.01)。高水平的HBA1C,HOME.IR,TCH和TG,以及低水平的胰岛素表明葡萄糖代谢与胰岛素抵抗不平衡;同时,较高的TCH和TG表明血脂血症也开发出来。在糖尿病小鼠保持高能量饮食中另外四周后,组织病理学观察显示心肌损伤,更高的表面积和胶原纤维,更高的LVHI和LV / BW,以及ANF mRNA的升高表达(P <0.01),表明在目前的实验条件下,Mus Musculus Castaneus小鼠出现了心肌肥大。因此,在糖尿病确认后4周建立了一种稳健的糖尿病心肌肥大模型,其通过喂养高脂饮食四周结合重复的低剂量STZ暴露,在Mus Musculus Castaneus小鼠中诱导。

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