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Assessing Functional Performance in the Mdx Mouse Model
Published on: March 27, 2014
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富含脂肪和糖的饮食会导致mdx小鼠的代谢变化
Swathy Krishna1, Kenneth G Echevarria2, Carter H Reed2
1Department of Animal Science, Iowa State University, Ames, Iowa, United States.
概括
一种高脂肪,高糖的饮食诱导肥胖/胰岛素抵抗在小鼠与杜申肌肉发育不良 (DMD),但没有恶化肌肉损伤. 这种饮食进一步损害了肌肉衰竭的代谢功能.
科学领域:
- 生物化学 生物化学
- 生理学 生理学 生理学
- 遗传学 是一个遗传学.
背景情况:
- 杜恩肌肉发育不良 (DMD) 是由于缺乏双蛋白而导致的,导致肌肉疾病和代谢问题.
- 肥胖和胰岛素抵抗 (O/IR) 在DMD患者中很常见,但它们对疾病严重性的影响尚不清楚.
研究的目的:
- 为了调查高脂肪,高糖饮食 (HFHSD) 是否会加剧DMD的严重程度并改变发育不良小鼠的新陈代谢.
- 为了确定饮食诱导的O/IR对肌肉损伤和代谢概况的影响,在双素缺乏的背景下.
主要方法:
- mdx小鼠 (DMD模型) 和野生型 (C57) 的小鼠被食控制饮食 (CD) 或HFHSD 15周.
- 评估了胰岛素耐药性,葡萄糖耐受性,内脏脂肪组织,血清肌酸激酶和隔膜组织学.
- 利用代谢和脂质组分析来评估代谢变化.
主要成果:
- 在两组小鼠中,HFHSD诱导了胰岛素耐药性,葡萄糖不耐受性和高血糖症;CD上的mdx小鼠也表现出胰岛素耐药性.
- 隔膜肌肉损伤归因于双素缺乏,而不是饮食.
- 代谢分析揭示了饮食诱导的变化,共同的基因型和独特的O / IR签名在dystrophin-deficient小鼠.
结论:
- 在mdx小鼠中,15周的HFHSD并没有使肌肉损伤恶化,但显著降低了代谢状态.
- 饮食诱导的O/IR在变质肌肉中带来了额外的代谢挑战,独立于肌肉损伤的明显恶化.
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