[1]张莎莎,孟杰杰,沈桂芬,等.肌肉生长抑制素前肽基因干预对高脂饮食诱导的肥胖小鼠脂代谢的影响[J].国际内分泌代谢杂志,2014,(06):361-364.[doi:10.3760/cma.j.issn.1673-4157.2014.06.001]
　Zhang Shasha*,Meng Jiejie,Shen Guifen,et al.Effects of myostatin propeptide gene intervention on dyslipidemia in high fat diet-induced obese mice[J].International Journal of Endocrinology and Metabolism,2014,(06):361-364.[doi:10.3760/cma.j.issn.1673-4157.2014.06.001]
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肌肉生长抑制素前肽基因干预对高脂饮食诱导的肥胖小鼠脂代谢的影响()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
期数:
2014年06期
页码:
361-364
栏目:
论著
出版日期:
2014-12-20

文章信息/Info

Title:
Effects of myostatin propeptide gene intervention on dyslipidemia in high fat diet-induced obese mice
作者:
张莎莎; 孟杰杰; 沈桂芬; 汪培华; 汪道文; 蒋建刚
430030 武汉,华中科技大学同济医学院附属同济医院心血管内科,高血压病研究所(张莎莎,孟杰杰,汪培华,汪道文,蒋建刚),风湿免疫科(沈桂芬); 孟杰杰现在沧州市人民医院心血管内二科
Author(s):
Zhang Shasha*;  Meng Jiejie;  Shen Guifen;  Wang Peihua;  Wang Daowen;  Jiang Jiangang.
*Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
关键词:
肌肉生长抑制素前肽;  肌肉生长抑制素;  高脂饮食;  肥胖
Keywords:
Myostatin propeptide;  Myostatin;  High fat diet;  Obesity
DOI:
10.3760/cma.j.issn.1673-4157.2014.06.001
文献标志码:
A
摘要:
目的 探讨肌肉生长抑制素前肽(MPRO)基因对高脂饮食诱导的肥胖小鼠脂代谢的影响及其分子机制。方法 60只雄性C57BL/6J小鼠按照随机数字表法分为4组(每组15只):正常对照组(NC组),高脂饮食组(HF组),高脂饮食+绿色荧光蛋白组(HF+GFP组)及高脂饮食+MPRO组(HF+MPRO组)。高脂饮食诱导肥胖小鼠模型,以重组腺相关病毒(rAAV)为载体介导MPRO基因或对照基因GFP在小鼠体内表达,观察并检测小鼠体重、皮下及内脏脂肪、血及肝脏甘油三酯水平的变化。Western印迹法检测肝脏AMP活化蛋白激酶α(AMPKα)、乙酰辅酶A羧化酶(ACC)、肉碱棕榈酰基转移酶-1(CPT-1)的表达情况。结果 HF组体重、皮下及内脏脂肪、血及肝脏甘油三酯水平较NC组显著升高(t=9.033～35.459,P均<0.05),HF+MPRO组体重、皮下及内脏脂肪、血及肝脏甘油三酯水平较HF组显著降低(t=5.233～21.500,P均<0.05)。Western印迹法显示HF组肝脏AMPKα、ACC磷酸化水平及CPT-1的表达较NC组显著降低(t=16.630～23.671,P均<0.05); HF+MPRO组肝脏AMPKα、ACC磷酸化水平、CPT-1的表达较HF组显著升高(t=8.143～10.314,P均<0.05)。结论 MPRO基因可能通过激活AMPK通路,明显改善肥胖小鼠的脂代谢紊乱。
Abstract:
ObjectiveTo investigate the effects and the associated molecular mechanism of myostatin propeptide(MPRO)gene intervention on dyslipidemia in high fat diet-induced obese mice. MethodsSixty C57BL/6J mice were divided into four groups according to the random number table(15 mice in each group): normal control group(NC group), high fat diet group(HF group), high fat diet+green fluorescent protein group(HF+GFP group)and high fat diet+MPRO group(HF+MPRO group). Mice were fed with high fat diet to induce obesity and dyslipidemia.Recombinant adeno-associated virus(rAAV)mediated MPRO or GFP gene were introduced to the mice, and their body weight, subcutaneous and visceral fat, as well as triglyceride in plasma and liver were measured. The expression of AMP-activated protein kinase α(AMPKα), acetyl-CoA carboxylase(ACC)and carnitine palmitoyltransferase-1(CPT-1)were detected by Western blot. ResultsCompared with NC group, body weight, subcutaneous and visceral fat, triglyceride in plasma and liver were significantly increased in HF group(t=9.033-35.459, all P<0.05). However, these were lower in HF+MPRO group than those in HF group(t=5.233-21.500, all P<0.05). Western blot demonstrated that compared with NC group, the phosphorylationof AMPKα and ACC as well as theexpression of CPT-1 were lower in HF group(t=16.630-21.502, all P<0.05). However, these were higher in HF+MPRO group than those in HF group(t=8.143-10.314, all P<0.05). Conclusion MPRO gene intervention attenuates dyslipidemia in obese mice partly through AMPK pathway.

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备注/Memo

备注/Memo:
基金项目:国家自然科学青年基金项目(30900694); 教育部留学服务中心回国基金项目(JYBHG201005)
更新日期/Last Update: 2015-11-19