Lipid accumulation mediated by adiponectin in C2C12 myogenesis.

Lipid accumulation mediated by adiponectin in C2C12 myogenesis.
复制标题

C2C12 肌生成中脂联素介导的脂质积累。

DOI:
10.5483/bmbrep.2009.42.10.667
复制
发表时间:
2009
期刊:
影响因子:
3.8
通讯作者:
Zaiqing Yang
Zaiqing Yang
中科院分区:
生物学3区
文献类型:
--
作者:
C. Yin;Q. Long;T. Lei;Xiaodong Chen;H. Long;B. Feng;Yin Peng;Yanling Wu;Zaiqing Yang

文献摘要

参考文献

相似文献

肥胖、心血管疾病、高血压和代谢综合征患者的血浆脂联素浓度降低。最近的研究发现脂联素可减少巨噬细胞泡沫细胞中的脂质积累,这可能会影响动脉粥样硬化的发展。然而,脂联素是否参与肌生成过程中的脂质积累过程仍不清楚。使用 C2C12 成肌细胞,我们研究了脂联素对成肌过程中肌细胞内脂质积累的影响。结果表明,C2C12分化过程中细胞内脂质积累显着减少,这显然是由于该过程中脂肪酸氧化增加和脂肪酸合成减少所致。与对照组相比,瞬时转染脂联素基因的 C2C12 细胞显示脂质积累减少。进一步的实验表明,脂联素可以通过增加 C2C12 肌生成过程中的脂肪酸氧化来抑制脂质积累。
Plasma concentrations of adiponectin have been shown to be decreased in patients with obesity, cardiovascular diseases, hypertension and metabolic syndrome. Recent studies have found that adiponectin reduces lipid accumulation in macrophage foam cells which may impact the development of atherosclerosis. However, it remains unclear whether adiponectin is involved in the process of lipid accumulation during myogenesis. Using C2C12 myoblasts, we investigated the effect of adiponectin on intramyocellular lipid accumulation during myogenesis. The results showed that intracellular lipid accumulation is significantly decreased during C2C12 differentiation, apparently due to increased fatty acid oxidation and decreased fatty acid synthesis during this process. C2C12 cells transiently transfected with adiponectin gene showed reduced lipid accumulation as compared to controls. Further experiments demonstrated that adiponectin can suppress lipid accumulation by increasing fatty acid oxidation during C2C12 myogenesis.
DOI: 10.1073/pnas.0403382101
发表时间: 2004-07-13
影响因子: 11.1
作者:
Hug, C;Wang, J;Lodish, HF
通讯作者: Lodish, HF
DOI: 10.1016/j.atherosclerosis.2008.04.011
发表时间: 2009-01-01
期刊: ATHEROSCLEROSIS
影响因子: 5.3
作者:
Tian, Ling;Luo, Nanlan;Fu, Yuchang
通讯作者: Fu, Yuchang
DOI: 10.1210/jcem.86.12.8075
发表时间: 2001-12
期刊: The Journal of clinical endocrinology and metabolism
影响因子: --
作者:
Bret H. Goodpaster;Jing He;Simon C. Watkins;David E. Kelley
通讯作者: Bret H. Goodpaster;Jing He;Simon C. Watkins;David E. Kelley