Effects of Cloprostenol administration on neutral lipid and prostaglandin F metabolism by porcine luteal tissue.
The effects of Cloprostenol administration on porcine luteal lipid metabolism, progesterone production, and prostaglandin F production were examined in 32 pigs at day 12 of the estrous cycle. Pigs were killed between 0 and 18 hours after treatment. Recovered luteal tissue was incubated at 0 C and at 37 C in the absence and presence of dibutyryl cyclic AMP and indomethacin. Net in vitro release of progesterone from luteal tissue was depressed within 1 hour after Cloprostenol treatment whereas net in vitro release of prostaglandin F was accelerated 4 hours after Cloprostenol treatment. Inclusion of dibutyryl cyclic AMP in the incubation media did not alter progesterone production but did enhance prostaglandin F production at 0 and 1 hour after Cloprostenol treatment. Inclusion of indomethacin in the incubation media completely inhibited the Cloprostenol-induced acceleration of in vitro luteal PGF production. Cloprostenol treatment increased luteal triglycerides and decreased luteal free cholesterol and cholesterol esters within 1 hr after treatment. Arachidonic acid percentages in free fatty acids and triglycerides were also increased within 1 hr after treatment. When 37 C and 0 C incubations were compared, in vitro luteal accumulation of free fatty acids was maximum at 1 hr after Cloprostenol treatment. In vitro accumulation of triglycerides in luteal tissue was comparatively uniform at all times examined during the first 18 hr after Cloprostenol treatment. Comparison of 37 C and 0 C incubations further revealed that luteal triglycerides were active in accumulation of arachidonic acid. Inclusion of dibutyryl cyclic AMP and/or indomethacin in the incubation media did not alter luteal lipid contents or fatty acid compositions. Blood plasma progesterone was depressed at 4 hours after Cloprostenol whereas 13,14-dihydro-15-keto-prostaglandin F2a was elevated at 18 hours after treatment. Blood plasma free fatty acids increased 330 percent at 4 hours and free fatty acid compositions also changed at this time. In both luteal tissue and blood plasma, changes in steroid and fatty acid metabolism occurred prior to changes in prostaglandin metabolism, suggesting that Cloprostenol induced functional luteal regression prior to altering prostaglandin metabolism.
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D003008:Cloprostenol / Q000494:pharmacology*; D003338:Corpus Luteum / Q000378:metabolism*; D000242:Cyclic AMP / Q000494:pharmacology; D015237:Dinoprost / Q000031:analogs & derivatives*; D004971:Estrus; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D050356:Lipid Metabolism; D011247:Pregnancy; D011374:Progesterone / Q000096:biosynthesis*; D011460:Prostaglandins F / Q000378:metabolism*; D011461:Prostaglandins F, Synthetic / Q000494:pharmacology*; D013552:Swine / Q000378:metabolism*; D013696:Temperature; D013997:Time Factors
D011460:Prostaglandins F; D011461:Prostaglandins F, Synthetic; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D003008:Cloprostenol; D011374:Progesterone; D003994:Bucladesine; D015237:Dinoprost; D000242:Cyclic AMP; D007213:Indomethacin