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 PGF(2α) but not of PGE2 as compared to cells incubated in normoxic conditions. Under hypoxia, the PLA2 inhibitor bromophenacyl bromide (BPB) inhibited AA release and PGF(2α) 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 elevated 5.1 ± 1.2 fold compared to control cells. Neither 10 μM BPB nor 100 mM aspirin (ASA) prevented this increase in GLUT1 expression. Preincubation of myotubes for either 1 or 23 h with 50 μM 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.
|Number of pages||6|
|Journal||Prostaglandins Leukotrienes and Essential Fatty Acids|
|State||Published - 1 Jan 1997|