Different effects of prostaglandins E2 and F2 alpha on triglyceride levels in uterine smooth muscle from diabetic diestrous rats.
Triglyceride (TG) concentrations in uterine strips isolated from diestrous normal rats, from diestrous streptozotocin (single iv. injection of 65 mg X Kg body weight-1)-diabetic rats and from diestrous diabetic animals, treated in vivo with insulin (protamine zinc insulin 4U X day-1, 6 days, sc.), were measured. Determinations were made immediately following killing (0 min, or postisolation) as well as after an incubation period in glucose-free medium (60 min, or postincubation), with or without additions. The basal or postisolation levels of TGs (0 min) in the uterus from control normal rats (TGs: 17.0 +/- 0.5 mumol X g-1, d.w.; blood glucose: 100.4 +/- 4.8 mg X dl-1) were lower (P less than 0.001) than in streptozotocin-diabetics (TGs: 28.5 +/- 0.6 mumol X g-1, d.w.; blood glucose: 302.0 +/- 10.1 mg X dl-1) and the treatment with insulin (blood glucose: 165.0 +/- 14.7 mg X dl-1), restored TGs towards normal (19.3 +/- 1.3 mumol X g-1, d.w.). The postisolation levels of TGs (0 min) in the uterus from normal controls did not differ in comparison with postincubation values (60 min), either without additions or in presence of indomethacin (5 X 10(-6)M) or of prostaglandins (PGs) E2 or F2 alpha, at 10(-9)M. On the contrary, in uteri from diabetic animals, the higher initial TG levels diminished spontaneously in comparison to controls (P less than 0.001) following 60 min of incubation without additions; this decrement being antagonized by indomethacin or by propranolol (10(-6)M). Moreover, exogenous PGE2 failed to alter the effect of indomethacin, whereas PGF2 alpha evoked its abolition. In addition, propranolol, which effectively blocked the spontaneous decrement of TGs as did indomethacin, prevented also the influence of PGF2 alpha on the action of the cyclo-oxygenase inhibitor. In the case of uteri from diabetic rats treated in vivo with insulin, TG levels remained unaltered at the end of an incubating period of 60 min without additions and so they did following the administration of indomethacin or PGF2 alpha. The results document that the regulation of TGs in the diestrous rat uteri, suspended in glucose-free solution, is affected differently by PGE2 and F2 alpha, depending on the existence or not of an untreated diabetic condition. They also suggest that the action of PGF2 alpha may involve the activation of tissue beta-adrenoreceptors.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D004031:Diestrus / Q000187:drug effects*; D015237:Dinoprost; D015232:Dinoprostone; D004971:Estrus / Q000187:drug effects*; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D007700:Kinetics; D009130:Muscle, Smooth / Q000187:drug effects / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D014280:Triglycerides / Q000378:metabolism*; D014599:Uterus / Q000187:drug effects / Q000378:metabolism*
D011458:Prostaglandins E; D011460:Prostaglandins F; D014280:Triglycerides; D011433:Propranolol; D015237:Dinoprost; D015232:Dinoprostone; D007213:Indomethacin