Efficacy and Side Effects of Low Single Doses of Cloprostenol Sodium or Dinoprost Tromethamine to Induce Luteolysis in Donkeys.

Due to the limited literature available evaluating doses of Prostaglandin F2α in donkeys, doses for horses have been extrapolated and used as guidelines. This study aimed to assess the efficacy and side effects of four different cloprostenol sodium and dinoprost tromethamine doses to induce luteolysis in jennies. Sixty-three cycles of seven Jennies (nine cycles per jenny) were used in this study. Seven days after ovulation, jennies randomly received one of the treatments in a crossover design as follows: Control, no treatment was administered; C1, 250 µg of cloprostenol sodium (CS, Estrumate , Merck Animal Health, USA); C2, 125 µg of CS; C3, 65.5 µg of CS, C4, 37.5 µg of CS; DT1, 5 mg of dinoprost tromethamine (DT, Lutalyse, Zoetis, USA); DT2, 2.5 mg of DT; DT3, 1.25 mg of DT; DT4, 0.625 mg of DT. Jennies were monitored for 30 minutes following treatment, and adverse effects were recorded. The measurement of the corpus luteum (CL) and the length of the estrous cycle were recorded. All DT and CS treatment doses were effective (P < .0001) in reducing the estrous cycle length compared to jenny's Control cycle. The CL volume was decreased in all treated groups one day after treatment (P < .05). The adverse effects were reduced as the dose of both Prostaglandin F2α analogs were reduced. In conclusion, a single low dose of dinoprost tromethamine (0.625 mg) or cloprostenol sodium (37.5 µg) can induce luteolysis and shorten the estrous length in jennies producing fewer adverse effects.

Fructose Synthesis and Transport at the Uterine-Placental Interface of Pigs: Cell-Specific Localization of SLC2A5, SLC2A8, and Components of the Polyol Pathway.

The fetal fluids and uterine flushings of pigs contain higher concentrations of fructose than glucose, but fructose is not detected in maternal blood. Fructose can be synthesized from glucose via enzymes of the polyol pathway, aldose reductase (AKR1B1) and sorbitol dehydrogenase (SORD), transported across cell membranes by solute carriers SLC2A5 and SLC2A8, and converted to fructose-1-phosphate by ketohexokinase (KHK). SLC2A8, SLC2A5, AKR1B1, SORD, and KHK mRNAs and proteins were analyzed using quantitative PCR and immunohistochemistry or in situ hybridization in endometria and placentae of cyclic and pregnant gilts, cyclic gilts injected with estrogen, and ovariectomized gilts injected with progesterone. Progesterone up-regulated SLC2A8 protein in uterine luminal (LE) and glandular epithelia during the peri-implantation period, and expression became exclusively placental, chorion and blood vessels, after Day 30. P4 up-regulated SLC2A5 mRNA in uterine LE and glandular epithelia after implantation, and the chorion expressed SLC2A5 between Days 30 and 85. AKR1B1 and SORD proteins localized to uterine LE during the peri-implantation period, but expression switched to chorion by Day 20 and was maintained through Day 85. Uterine expression of AKR1B1 mRNA was down-regulated by estrogen. KHK protein localized to trophectoderm/chorion throughout gestation. These results provide evidence that components for the conversion of glucose to fructose and for fructose transport are present at the uterine-placental interface of pigs. The shift in expression from LE to chorion during pregnancy suggests free-floating conceptuses are supported by fructose synthesized by the uterus, but after implantation, the chorion becomes self-sufficient for fructose synthesis and transport.