Kozlovsky N, Shohami E, Bashan N
Pediatric Research Laboratory, Soroka Medical Center, Beer-Sheva, Israel.
Prostaglandins Leukot Essent Fatty Acids. 1997 Jan;56(1):17-22. doi: 10.1016/s0952-3278(97)90520-2.
Incubation of L6 myotubes for 24 h under hypoxic conditions leads to a 5.8 +/- 1.2 fold increase in 2-deoxyglucose uptake. In those conditions phospholipase A2 is activated, leading to a 2.4 +/- 0.8 fold increased release of arachidonic acid (AA) to the medium, and to 95% increased synthesis of PGF2 alpha but not of PGE2 as compared to cells incubated in normoxic conditions. Under hypoxia, the PLA2 inhibitor bromophenacyl bromide (BPB) inhibited AA release and PGF2 alpha synthesis, yet it did not affect the increase in glucose uptake into L6 myotubes. The amount of GLUT1 immunoreactive proteins in total membranes of hypoxia treated cells was evaluated 5.1 +/- 1.2 fold compared to control cells. Neither 10 microM BPB nor 100 mM aspirin (ASA) prevented this increase in GLUT1 expression. Preincubation of myotubes for either 1 or 23 h with 50 microM exogenous AA, prevented insulin induced 2-deoxyglucose uptake stimulation, suggesting that although AA or one of its metabolites did not regulate the synthesis or stability of GLUT1, it may interfere with the signal transduction of insulin in muscle cells.
在缺氧条件下将L6肌管培养24小时，会导致2-脱氧葡萄糖摄取增加5.8±1.2倍。在这些条件下，磷脂酶A2被激活，导致花生四烯酸（AA）释放到培养基中的量增加2.4±0.8倍，与在常氧条件下培养的细胞相比，PGF2α的合成增加95%，而PGE2的合成没有增加。在缺氧条件下，磷脂酶A2抑制剂溴苯甲酰溴（BPB）抑制了AA的释放和PGF2α的合成，但它不影响L6肌管对葡萄糖摄取的增加。与对照细胞相比，缺氧处理细胞总膜中GLUT1免疫反应蛋白的量评估为增加5.1±1.2倍。10 microM的BPB和100 mM的阿司匹林（ASA）均不能阻止GLUT1表达的这种增加。用50 microM外源AA对肌管进行1小时或23小时的预孵育，可阻止胰岛素诱导的2-脱氧葡萄糖摄取刺激，这表明尽管AA或其一种代谢产物不调节GLUT1的合成或稳定性，但它可能会干扰胰岛素在肌肉细胞中的信号转导。
