Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100191, China.
Molecules. 2012 Jun 11;17(6):7083-92. doi: 10.3390/molecules17067083.
We investigated the effects of Astragalus polysaccharide (APS) on palmitate-induced insulin resistance in C2C12 skeletal muscle myotubes. Palmitate-reduced glucose uptake was restored by APS. APS prevented palmitate-induced C2C12 myotubes from impaired insulin signaling by inhibiting Ser307 phosphorylation of insulin receptor substrate-1 (IRS-1) and increasing Ser473 phosphorylation of Akt. Moreover, the increases in protein-tyrosine phosphatase-1B (PTP1B) protein level and NF-κB activation associated with palmitate treatment were also prevented by APS. However the treatment with APS didn't change AMP-activated protein kinase (AMPK) activation in palmitate-induced myotubes. The results of the present study suggest that Astragalus polysaccharide inhibits palmitate-induced insulin resistance in C2C12 myotubes by inhibiting expression of PTP1B and regulating NF-κB but not AMPK pathway.
我们研究了黄芪多糖 (APS) 对棕榈酸诱导的 C2C12 骨骼肌肌管胰岛素抵抗的影响。APS 恢复了棕榈酸降低的葡萄糖摄取。APS 通过抑制胰岛素受体底物-1 (IRS-1) 的 Ser307 磷酸化和增加 Akt 的 Ser473 磷酸化，防止棕榈酸诱导的 C2C12 肌管胰岛素信号受损。此外，还可以防止与棕榈酸盐处理相关的蛋白酪氨酸磷酸酶-1B（PTP1B）蛋白水平和 NF-κB 激活的增加。然而，APS 处理并没有改变棕榈酸诱导的肌管中 AMP 激活的蛋白激酶 (AMPK) 的激活。本研究结果表明，黄芪多糖通过抑制 PTP1B 的表达和调节 NF-κB 而不是 AMPK 途径来抑制 C2C12 肌管中棕榈酸诱导的胰岛素抵抗。
