The highly seasonal anadromous Arctic charr (Salvelinus alpinus) was used to investigate the possible involvement of altered gene expression of brain neuropeptides in seasonal appetite regulation. Pro-opiomelanocortin (POMCA1, POMCA2), Cocaine and amphetamine regulated transcript (CART), Agouti related Peptide (AgRP), Neuropeptide Y (NPY) and Melanocortin Receptor 4 (MC4-R) genes were examined. The function of centrally expressed Leptin (Lep) in fish remains unclear, so Lep (LepA1, LepA2) and Leptin Receptor (LepR) genes were included in the investigation. In a ten months study gene expression was analysed in hypothalamus, mesencephalon and telencephalon of immature charr held under natural photoperiod (69°38’N) and ambient temperature and given excess feed. From April to the beginning of June the charr did not feed and lost weight, during July and August they were feeding and had a marked increase in weight and condition factor, and from November until the end of the study the charr lost appetite and decreased in weight and condition factor. Brain compartments were sampled from non-feeding charr (May), feeding charr (July), and non-feeding charr (January). Reverse transcription real-time quantitative PCR revealed temporal patterns of gene expression that differed across brain compartments. The non-feeding charr (May, January) had a lower expression of the anorexigenic LepA1, MC4-R and LepR in hypothalamus and a higher expression of the orexigenic NPY and AgRP in mesencephalon, than the feeding charr (July). In the telencephalon, LepR was more highly expressed in January and May than in July. These results do not indicate that changes in central gene expression of the neuropeptides investigated here directly induce seasonal changes in feeding in Arctic charr.

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Background The Arctic charr ( Salvelinus alpinus ) has a highly seasonal feeding cycle that comprises long periods of voluntary fasting and a short but intense feeding period during summer. Therefore, the charr represents an interesting species for studying appetite-regulating mechanisms in fish. Results In this study, we compared the brain transcriptomes of fed and feed deprived charr over a 4 weeks trial during their summer feeding season. Despite prominent differences in body condition between fed and feed deprived charr at the end of the trial, feed deprivation affected the brain transcriptome only slightly. In contrast, the transcriptome differed markedly over time in both fed and feed deprived charr, indicating strong shifts in basic cell metabolic processes possibly due to season, growth, temperature, or combinations thereof. The GO enrichment analysis revealed that many biological processes appeared to change in the same direction in both fed and feed deprived fish. In the feed deprived charr processes linked to oxygen transport and apoptosis were down- and up-regulated, respectively. Known genes encoding for appetite regulators did not respond to feed deprivation. Gene expression of Deiodinase 2 ( DIO2 ), an enzyme implicated in the regulation of seasonal processes in mammals, was lower in response to season and feed deprivation. We further found a higher expression of VGF (non-acronymic) in the feed deprived than in the fed fish. This gene encodes for a neuropeptide associated with the control of energy metabolism in mammals, and has not been studied in relation to regulation of appetite and energy homeostasis in fish. Conclusions In the Arctic charr, external and endogenous seasonal factors for example the increase in temperature and their circannual growth cycle, respectively, evoke much stronger responses in the brain than 4 weeks feed deprivation. The absence of a central hunger response in feed deprived charr give support for a strong resilience to the lack of food in this high Arctic species. DIO2 and VGF may play a role in the regulation of energy homeostasis and need to be further studied in seasonal fish. Electronic supplementary material The online version of this article (10.1186/s12864-019-5874-z) contains supplementary material, which is available to authorized users.