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Establishment of a diabetic myocardial hypertrophy model in Mus musculus castaneus mouse

机译:小家鼠糖尿病性心肌肥大模型的建立

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摘要

The aim of this study was to establish a robust model of diabetic myocardial hypertrophy in mice. Mice were fed a high‐fat diet for four weeks and then given streptozotocin (STZ, 40 mg kg  d 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 ( < 0.01). 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 ( < 0.01), suggesting that myocardial hypertrophy had appeared in 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 mice.
机译:这项研究的目的是建立一种小鼠糖尿病心肌肥大的鲁棒模型。给予小鼠高脂饮食四周,然后给予链脲佐菌素(STZ,40 mg / kg,持续5天,腹腔注射),并在7天后测试空腹血糖(FBG)水平。 FBG水平高于11.1 mmol / L的小鼠被认为患有糖尿病。糖尿病小鼠继续获得高脂饮食,直到出现心脏肥大。每周测量FBG和体重(BW)。通过左心室肥大指数(LVHI),LV / BW,LV组织病理学观察和心房利钠因子(ANF)mRNA表达来确认心肌肥大。测量血清胰岛素和血浆血红蛋白A1c(HbA1c)水平,总胆固醇(TCH)和甘油三酸酯(TG),然后计算胰岛素抵抗指数(HOMA.IR)。与对照组相比,模型组的FBG水平保持在11.1 mmol / L以上,并且BW表现出明显的体重减轻。 HbA1c,HOME.IR,TCH和TG的高水平以及胰岛素的低水平表明葡萄糖代谢与胰岛素抵抗不平衡。同时,较高的TCH和TG表明血脂异常也已发展。糖尿病小鼠继续高能量饮食四个星期后,组织病理学观察显示心肌损伤,更多的表面积和胶原纤维,更高的LVHI和LV / BW以及ANF mRNA表达升高(<0.01),提示在目前的实验条件下,小鼠已经出现心肌肥大。因此,在确认糖尿病后4周建立了一个强有力的糖尿病心肌肥大模型,这是通过在小鼠中喂食高脂饮食4周并反复重复低剂量STZ暴露而诱发的。

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