Oleate protects against palmitate-induced insulin resistance in L6 myotubes

Oleate protects against palmitate-induced insulin resistance in L6 myotubes
复制标题

DOI:
10.1017/s0007114509990948
复制
发表时间:
2009-12-14
影响因子:
3.6
通讯作者:
Bailey, Clifford J.
Bailey, Clifford J.
中科院分区:
医学3区
文献类型:
--
作者:
Gao, Dan;Griffiths, Helen R.;Bailey, Clifford J.

文献摘要

被引文献

相似文献

油酸盐已被证明可以预防棕榈酸诱导的胰岛素抵抗。本研究探讨了油酸和棕榈酸在L6骨骼肌细胞胰岛素刺激的葡萄糖摄取中相互作用的机制。L6肌管分别与棕榈酸或油酸、棕榈酸与油酸联合培养6h,并加或不加磷脂酰肌醇3-激酶(PI3-K)抑制。胰岛素刺激的葡萄糖摄取。通过摄取2-脱氧-D-[H-3]葡萄糖来衡量,30亩棕榈酸酯几乎完全阻止了这一过程。当油酸浓度达到750mU/L时,细胞对胰岛素刺激的葡萄糖摄取量显著增加。50-300亩M-油酸盐与300亩M-棕榈酸酯共同孵育,部分地阻止了与棕榈酸酯相关的胰岛素刺激的葡萄糖摄取的减少。在50亩油酸+300亩棕榈酸酯中加入PI3-激酶抑制剂Wortmannin(10(-7)m ol/L)或LY294002(25 m o l/L)可显著降低油酸对棕榈酸诱导的胰岛素抵抗的有利作用,提示PI3-激酶的激活参与了油酸的保护作用。因此,油酸对L6肌细胞中棕榈酸诱导的胰岛素抵抗的预防作用与油酸通过PI3-激酶维持胰岛素信号的能力有关。
Oleate has been shown to protect against palmitate-induced insulin resistance. The present Study investigates mechanisms involved in the interaction between oleate and palmitate on insulin-stimulated glucose uptake by L6 skeletal muscle cells. L6 myotubes Were Cultured for 6h with palmitate or oleate alone, and combinations of palmitate with oleate, with and without phosphatidylinositol 3-kinase (PI3-kinase) inhibition. Insulin-stimulated glucose uptake. measured by uptake of 2-deoxy-D-[H-3]glucose, was almost completely prevented by 30 mu M-palmitate. Cells incubated with oleate up to 750 mu mol/l maintained a significant increase in insulin-stimulated glucose uptake. Co-incubation of 50-300 mu M-oleate with 300 mu M-palmitate partially prevented the decrease in insulin-stimulated glucose uptake associated with palmitate. Adding the PI3-kinase inhibitors wortmannin (10(-7) mol/l) or LY294002 (25 mu mol/l) to 50 mu M-oleate plus 300 mu M-palmitate significantly reduced the beneficial effect of oleate against palmitate-induced insulin resistance, indicating that activation of PI3-kinase is involved in the protective effect of oleate. Thus, the prevention of palmitate-induced insulin resistance by oleate in L6 muscle cells is associated with the ability of oleate to maintain insulin signalling through PI3-kinase.