Abstract
The effects of platelet activating factor (PAF) on glucose oxidation in uterine strips isolated from rats in the 4 th and 5 th day of pregnancy, were explored. PAF, at a concentration of 10 −10 and 10 −8 M, augmented significantly the generation of 14CO 2 from labelled glucose in uteri from pregnant rats in the 4 th day of pregnancy. When the tissue was obtained from 5 days pregnant rats, the addition of PAF at 10 −8 increased significantly more than PAF at 10 −10 M the metabolism of glucose. On the other hand, PAF at 10 −8 M failed to alter the uterine basal production of 14CO 2 from labelled glucose in animals at estrus. BN52021, a specific PAF antagonist employed at 10 −5 M, blocked completely the action of PAF in the pregnant rat uterus. PGE 1, PGE 2 and PGF 2α enhanced significantly the formation of 14CO 2 from labelled glucose in uteri from 5 days pregnant rats. Indomethacin, a well known inhibitor of prostaglandin synthesis, did not alter the basal glucose metabolism in uteri from 5 days pregnant rats, but antagonized completely the stimulating action of PAF on 14CO 2 production from labelled glucose an effect that was partially reverted by the addition of PGE 1, PGE 2 or PGF 2α (10 −7 M). Furthermore, nordihydroguaiaretic acid (NDHGA), a specific inhibitor of 5-lipoxygenase at 10 −5 M, as well as FPL-55712, an antagonist of leukotrienes (LTs), at the same concentration, blocked the action of PAF on the metabolism of glucose. The action of NDHGA was partially counteracted by the addition of LTC 4 at 10 −7 M. Considering all these results, we suggest that PAF stimulates indirectly glucose metabolism via the “de novo” synthesis of PGs anb LTs, probably by the activation of phospholipase A 2 (PLA 2). As far as we know the present report represent the first description of a stimulating action of PAF on glucose metabolism in pregnant rat uteri.
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