Tryglycerides in isolated rat uterine strips. Influences of glucose deprivation, 2-deoxy-D-glucose, estrogens and exogenous or endogenous prostaglandins E 1, E 2 and F 2α

Abstract

Triglyceride (TG) levels in uterine strips isolated from natural estrous, ovariectomized or ovariectomized, estradiol-injected rats, were explored. Determinations were performed either immediately after isolation (initial or 0 time) as well as after one hour period of incubation (60 min time) in glucose containing or in glucose-free solution. The influences of indomethacin alone (5×10 −6M) or of ondomethacin plus prostaglandins (PGs) E 2,E 1 or F 2α (10 −7M). delivered in vitro at the beginning of the incubation, and of 2-deoxy-D-glucose 2-DG) at 11.0 mM, were also studied. Ovariectomized animals (25 days); estrous animals or spayed 17-beta estradiol-injected animals (0.5 ug + 1.0 ug, 24 hours prior to sacrifice), were employed. At 60 min time in glucose-free medium, but not in glucose containing solution, triglycerides declined significantly in strips fron spayed rats, the diminution being prevented by in vitro indomethacin. The presence of exogenous PGF 2 a Or of PGE 1, but not that of PGE 2, abolished the pteventive effect of indomethacin. Initial TG levels in spayed uteri treated with estradiol were significantly smaller that in untreated controls. However, under these conditions, indomethacin alone or indomethacin plus the tested PGs, had no action, the same being evident at natural estrus. In strips from spayed rats and incubated in the absence of glucose but with the presence of 2-DG, the effects of indomethacin and of indomethacin plus exogenous PGs on tissue TG levels were similar, although more evident, than in the sole absence of extracellular glucose. Moreover, TG levels in uterine strips obtained from ovariectomized rats injected with 17-beta estradiol and incubated for 60 min in glucose-free medium plus 2-DG, were smaller than immediately after isolation (0 time), the decrement being prevented by indomethacin, not affected by PGE 2, and abolished by PGE 1, or by PGF 2α The foregoing results suggest that the diminution of TG in uterine strips incubated in the absence of glucose could be due to a greater metabolic utilization of neutral fats, a phenomenon possibly associated to the lack of exogenous substrate. Moreover, this decrement of tissue TG apeears to be linked to the influence of certain PGs and of estrogens, for in ovariectomized, but not in estrous or in spayed-estrogenized conditions, indomethacin prevented the TG decrement in glucose-free solution, whereas PGs E 1 and PGF 2α abolished the preventive action of indomethacin. Moreover, under the combination of substrate-free condition plus the presence of 2-DG, an inhibitor of glucose transport and tissue glycolysis, uteri from both ovariectomized or spayed-estrogenized rats, reacted to the addition of indomethacin with an abolition of TG decrement, and PGs E 1 or F 2α , but not PGE 2, blunted the influence of indomethacin. This would imply a definite influence of endogenous carbohydrate metabolism and of some PGs on tissue TG levels, both under estrogen or non-estrogen dominance.