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首页> 外文期刊>Experimental Animals >Type 2 Diabetes Mellitus in a Non-Obese Mouse Model Induced by Meg1/Grb10 Overexpression
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Type 2 Diabetes Mellitus in a Non-Obese Mouse Model Induced by Meg1/Grb10 Overexpression

机译：Meg1 / Grb10过表达诱导的非肥胖小鼠模型中的2型糖尿病

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We assessed the possibility of C57BL/6-Tg (Meg1/Grb10)isn(Meg1 Tg) mice as a non-obese type 2 diabetes (2DM) animal model. Meg1 Tg mice were born normal, but their weight did not increase as much as normal after weaning and showed about 85% of normal size at 20 weeks of age. Body mass index of Meg1 Tg mice was also smaller than that of control mice. The glucose tolerance test and insulin tolerance test showed that Meg 1 Tg mice had reduced ability to normalize the blood glucose level. Blood urea nitrogen (BUN) in Meg1 Tg mice (19.6 ± 1.2 mg/dl) was significantly lower than in controls (22.0 ± 0.8 mg/ dl), while plasma triglyceride, insulin, adiponectin, and resistin levels were significantly higher (202.0 ± 23.4 mg/dl vs 146.3 ± 23.4 mg/dl, 152.4 ± 16.3 pg/ml vs 88.1 ±16.9 pg/ml, 74.4 ± 10.9 μg/ml vs 48.3 ± 7.0 μg/ml, and 4.0 ± 0.2 ng/ml vs 3.6 ± 0.2 ng/ml, respectively). Body, visceral fat weight and liver weights were significantly lower (19.6 ± 0.4 g vs 24.3 ± 0.3 g, 376.7 ± 29.6 mg to 507.5 ± 23.0 mg, and 906.0 ± 41.8 mg to 1,001.0 ± 15.1 mg, respectively). Thus, hyperinsulinemia observed in Meg1 Tg mice indicates that their insulin signaling pathway is somehow inhibited. With high fat diet, the diabetes onset rate of Meg1 Tg mice increased up to 60%. These results suggest that Meg1 Tg mice resemble human 2DM.
机译：我们评估了C57BL / 6-Tg（Meg1 / Grb10）isn（Meg1 Tg）小鼠作为非肥胖2型糖尿病（2DM）动物模型的可能性。 Meg1 Tg小鼠出生时正常，但断奶后体重没有像正常人那样增加，并且在20周龄时显示出正常体重的约85％。 Meg1 Tg小鼠的体重指数也小于对照组。葡萄糖耐量试验和胰岛素耐量试验表明，Meg 1 Tg小鼠的血糖正常化能力降低。 Meg1 Tg小鼠的血尿素氮（BUN）（19.6±1.2 mg / dl）显着低于对照组（22.0±0.8 mg / dl），而血浆甘油三酸酯，胰岛素，脂联素和抵抗素水平显着较高（202.0± 23.4 mg / dl与146.3±23.4 mg / dl，152.4±16.3 pg / ml与88.1±16.9 pg / ml，74.4±10.9μg/ ml与48.3±7.0μg/ ml和4.0±0.2 ng / ml与3.6±分别为0.2 ng / ml）。身体，内脏脂肪重量和肝脏重量显着降低（分别为19.6±0.4 g和24.3±0.3 g，376.7±29.6 mg至507.5±23.0 mg和906.0±41.8 mg至1,001.0±15.1 mg）。因此，在Meg1 Tg小鼠中观察到的高胰岛素血症表明其胰岛素信号传导途径受到了某种抑制。使用高脂饮食，Meg1 Tg小鼠的糖尿病发病率增加了60％。这些结果表明，Meg1 Tg小鼠类似于人2DM。

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