| Talk title | Spexin as a Novel Regulator for Feeding Control and Reproduction in Fish Mode |
| Speaker | Prof. Anderson O.L. WONG Professor School of Biological Sciences, University of Hong Kong |
| Date & Time | 02 January 2019 (Wed) 15:00-16:00 |
| Venue | Room 4004, E12 Building (University of Macau) |
| Abstract | Spexin (SPX), a neuropeptide with pleiotropic functions, has been identified as a satiety factor in fish models. In our recent study with goldfish, insulin was confirmed to be a functional link between food intake and SPX expression in the liver and IGF-I receptor (IGF1R) together with insulin receptor (InsR) were found to be involved in insulin-induced SPX expression at the hepatic level, which raises the possibility that the hepatic signal of insulin-like growth factor (IGF) induced by growth hormone (GH) may play a role in SPX regulation. In this study, food intake in goldfish was found to up-regulate plasma levels of insulin, SPX and GH with parallel rises of GH mRNA in the pituitary and transcript expression of SPX, IGF-I and IGF-II in the liver. In goldfish pituitary cells, insulin treatment could induce GH secretion without notable changes in GH mRNA expression. In goldfish hepatocytes, GH induction could increase SPX, IGF-I and IGF-II gene expression via activation of JAK2/STAT5, MEK1/2/ERK1/2 and PI3K/Akt pathways and these stimulatory effects were blocked by inhibiting InsR and IGF1R activation. Interestingly, parallel treatment with insulin was shown to up-regulate IGF-I with concurrent inhibition on IGF-II mRNA expression and these differential effects were mediated by PI3K/ Akt but not MAPK cascades. Meanwhile, insulin-induced IGF-I gene expression was additive to the corresponding stimulation by GH but the parallel rise of IGF-II mRNA induced by GH could be suppressed by insulin co-treatment. At hepatocyte level, IGF-I and IGF-II were both effective in stimulating SPX mRNA expression mainly through InsR, and to a lesser extent via IGF1R, by functional coupling to P38 MAPK and PI3K/Akt pathways. These results, as a whole, indicate that insulin can induce SPX expression in goldfish liver via indirect action of GH/IGF axis and local production of IGF-I/-II. Since insulin signal triggered by feeding is known to be transient mainly due to the signal termination by glucose homeostasis, the IGF-I/-II expression at hepatic level may play a role in prolonging/maintaining the SPX responses after food intake in fish model. |