This investigation aimed to assess the appetite response changes of olive flounder to starving and re-feeding conditions. Three different feeding groups (2 weeks feeding, fed; 2 weeks starving, starved; and 1 week starving and 1 week feeding, re-fed) were established to examine the changes in appetite-related genes for each group. The weight gain of the fish was highest for the fed group and lowest for the starving group. Based on the daily feed intake (DFI) and cumulative feed intake (CFI), overall food intake was found to increase in the re-fed group more than in the fed group from week 1 to week 2 of the experiment. Hypocretin neuropeptide precursor (HCRT) and galanin receptor 1 (GAL-R1) mRNA expression in the brain of olive flounder were decreased in the starved group. Corticotropin-releasing hormone (CRH) was decreased in all experimental groups, except for the fed group. However, overall leptin concentrations in the plasma did not change across groups. Considering the differences between this study and previous studies on starving and feeding, various factors (except the production and expression mechanisms of appetite-related factors in response to starving) are likely acting on the appetite responses of the fish. In this study, a 1-week re-feeding period induced substantial effects on appetite response when compared to a 2-week feeding period. These findings show that even if re-feeding is performed after starving, the unbalance caused by the re-feeding can affect various physiological changes in fish by feed intake efficiency.

We investigated the effect of light spectra on circadian rhythm by exogenous prolactin (PRL) by using light emitting diodes (LEDs): red, green, and purple. We injected PRL into live fish or treated cultured brain cells with PRL. We measured changes in the expressions of period 2 (Per2), cryptochrome 1 (Cry1), melatonin receptor 1 (MT1) mRNAs, and MT1 proteins, and in the plasma PRL, serotonin, and melatonin levels. After PRL injection and exposure to green LED light, MT1 expression and plasma melatonin levels were significantly lower, but the expressions of Per2 and Cry1 were significantly higher than others. Plasma serotonin after PRL injection and exposure to red LED light was significantly lower than others. These results indicate that injection of high concentration PRL inhibits melatonin, and inhibited melatonin regulates circadian rhythm via clock genes and serotonin. Thus, exogenous PRL regulates the circadian rhythm and light spectra influence the effect of PRL in goldfish.

In particular, maternal prostacyclin (PGI2) is critical for embryo implantation and the action of PGI2 is not mediated via its G protein-coupled membrane receptor, IP, but its nuclear receptor, peroxisome proliferator-activated receptor δ (PPARδ). Recently, several studies have shown that PGI2 enhances blastocyst development and/or hatching rate in vitro, and subsequently implantation and live birth rates in mice. However, the mechanism by which PGI2 improves preimplantation embryo development in vitro remains unclear. Using molecular, pharmacologic and genetic approaches, we show that PGI2-induced PPARδ activation accelerates blastocyst hatching in mice. mRNAs for PPARδ, RXRs (heterodimeric partners of PPARδ) and PGI2 synthase are temporally induced after zygotic gene activation and their expression reaches maximum levels at the blastocyst stage, suggesting that functional complex of PPARδ can be formed in the blastocyst. Carbaprostacyclin (cPGI, a stable analogue of PGI2) and GW501516 (a PPARδ selective agonist) significantly accelerated blastocyst hatching but did not increase total cell number of cultured blastocysts. Whereas U51605 (a PGIS inhibitor) interfered with blastocyst hatching, GW501516 restored U51605-induced retarded hatching. In contrast to improvement of blastocyst hatching by PPARδ agonists, PPAR antagonists significantly inhibited blastocyst hatching. Furthermore, deletion of PPARδ at early stages of preimplantation mouse embryos caused delay of blastocyst hatching, but did not impair blastocyst development. Taken together, PGI2-induced PPARδ activation accelerates blastocyst hatching in mice.