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Glucokinase gene locus transgenic mice are resistant to the development of obesity-induced type 2 diabetes

机译:葡萄糖激酶基因基因座转基因小鼠对肥胖诱导的2型糖尿病的发生有抵抗力

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Transgenic mice that overexpress the entire glucoki- nase(GK)gene locus have been previously shown to be midly hypoglycemic and to have improved tolerance to glucose. To determine whether increased GK might also prevent or diminish diabetes in diet-induced obese ani- mals, we examined the effect of feeding these mice a high-fat high-simple carbohydrate low-fiber diet(HF diet)for 30 weeks. In response to this diet, both normal and transgenic mice became obese and had similar BMIs (5.3±0.1 and 5.0±0.1 kg/m~2)in transgenic and non- transgenic mice, respectively.
机译:过表达整个葡糖激酶(GK)基因位点的转基因小鼠先前已被证明具有中等程度的降血糖作用,并且对葡萄糖的耐受性得到了改善。为了确定GK的增加是否也可以预防或减少饮食引起的肥胖动物的糖尿病,我们研究了给这些小鼠喂食高脂肪高简单碳水化合物低纤维饮食(HF饮食)持续30周的效果。响应于这种饮食,正常和转基因小鼠均变得肥胖,并且在转基因和非转基因小鼠中分别具有相似的BMI(5.3±0.1和5.0±0.1kg / m〜2)。

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