Zhang Liu, Ma Huijuan, Xing Hanying, et al. Role of STARS in insulin resistance induced by palmitic acid in muscle cells[J]. Journal of Chongqing Medical University, 2017,42(11):1503-1508.
Zhang Liu, Ma Huijuan, Xing Hanying, et al. Role of STARS in insulin resistance induced by palmitic acid in muscle cells[J]. Journal of Chongqing Medical University, 2017,42(11):1503-1508. DOI: 10.13406/j.cnki.cyxb.001404.
PA组STARS m RNA和蛋白的表达明显增加(均P=0.000);STARS上调组肌细胞STARS m RNA和蛋白表达均明显增加(均P=0.000)
IRS-1(P=0.000)、GLUT4(P=0.000)和AKT m RNA(P=0.000)表达明显下降
AKT丝氨酸磷酸化水平(P=0.000)和GLUT4(P=0.000)蛋白的表达显著降低
IRS-1丝氨酸磷酸化水平显著增加。下调STARS的表达后出现了与上述相反的结果。经上述干预后
SRF和MKL1基因和蛋白水平均没有明显变化。结论:STARS与胰岛素敏感性密切相关
但其下游靶点MKL1和SRF没有变化。可能通过影响其修饰后翻译
也可能通过其他信号通路在胰岛素抵抗中发挥作用
需要进一步研究。
Abstract
Objective:To study the role of the striated muscle activator of Rho signaling(STARS)in insulin resistance induced by palmitic acid in muscle cells as well as the potential mechanisms modulating STARS expression. Methods:L6 myoblasts were incubated with palmitic acid to establish a model for insulin resistance. The effects of STARS on insulin resistance in L6 muscle cells were observed and its potential mechanisms of action were further explored by inducing its over-expression and knockdown. Levels of STARS
SRF
MKL1
AKT
IRS-1 and GLUT4 m RNA and protein were detected by RT-PCR and Western blot
respectively. Results:Compared with those in the control group
STARS m RNA and protein levels were significantly increased in muscle cells in the PA(palmitic acid)and pc DNA/STARS(STARS over-expression)groups. Levels of IRS-1
GLUT4 and AKT m RNA were significantly decreased in the pc DNA/STARS group. In addition
serine phosphorylation of AKT and GLUT4 protein levels were decreased and serine phosphorylation of IRS-1 was increased. In contrast
STARS knockdown produced the opposite results in above parameters. MKL1 and SRF m RNA and protein levels were unaffected by these interventions. Conclusion:STARS is closely related with insulin sensitivity
while without significant changes of its downstream target MKL1 and SRF. It might play a role in insulin resistance by modulating post-translational modification of MKL1 and SRF or through other signaling pathways. Further investigations are thus needed.