Feedback from Arctic charr: Feed flavour stimulation and re-feeding after feed deprivation stimulate genes encoding both orexigenic and anorexigenic neuropeptides.

Despite vast research attention, the knowledge about central mechanisms of appetite regulation in teleost remains inconclusive. A common strategy in studies on appetite regulating mechanisms is to measure the response to feed restriction or - deprivation, but responses vary between fish species and between experiments, and are also likely dependent on the degree of energy perturbation. The anadromous Arctic charr is an interesting model for studying appetite regulation as its feeding cycle comprises months of winter anorexia, and hyperphagia during summer. Here we studied how the gene expression of putative hypothalamic appetite regulators were affected by two days, one week and one month feed deprivation during summer, and subsequent re-feeding and exposure to feed flavour. Short-term feed deprivation caused only a minor reduction in condition factor and had no effect on hypothalamic gene expression. Long-term feed-deprivation caused a marked reduction in weight and condition factor which contrasted the increase in weight and condition factor seen in ad libitum fed controls. A marked energy perturbation by feed deprivation was also indicated by a lower hypothalamic expression of the genes encoding insulin-like growth factor 1 (IGF1) and IGF1 binding protein 5 in the feed deprived charr compared to fed controls. Surprisingly, long-term feed deprivation and energy perturbation did not induce changes in hypothalamic appetite regulators. Unexpectedly, re-feeding and exposure to feed flavour caused an increase in the expression of the genes encoding the orexigenic agouti-related peptide and the anorexigenic melanocortin receptor 4 and cocaine- and amphetamine-regulated transcript. Our study gives strong evidence for a role of these in appetite regulation in Arctic charr, but their mechanisms of action remain unknown. We suggest that changes in gene expression are more likely to be registered during transition phases, e.g. from fasting to feeding and upon stimulatory inputs such as feed flavour.

Effect of long-term fasting and a subsequent meal on mRNA abundances of hypothalamic appetite regulators, central and peripheral leptin expression and plasma leptin levels in rainbow trout.

Knowledge about neuroendocrine mechanisms regulating appetite in fish, including the role of leptin, is inconclusive. We investigated leptin mRNA abundance in various tissues, plasma leptin levels and the hypothalamic gene expression of putative orexigenic (neuropeptide Y and agouti-regulated peptide) and anorexigenic (melanocortin receptor, proopiomelanocortins (POMCs), cocaine- and amphetamine-regulated transcript and corticotropin-releasing factor) neuropeptides in relation to feeding status in rainbow trout (Oncorhynchus mykiss). Blood and tissues were first (Day 1) sampled from trout that had been fed or fasted for 4 months and the day after (Day 2) from fasted fish after they had been given a large meal, and their continuously fed counterparts. The fasted fish ate vigorously when they were presented a meal. There were no differences between fed, fasted and re-fed fish in hypothalamic neuropeptide transcript levels, except for pomca1 and pomcb, which were higher in fasted fish than in fed fish at Day 1, and which, for pomcb, decreased to the level in fed fish after the meal at Day 2. Plasma leptin levels did not differ between fasted, re-fed and fed fish. A higher leptina1 transcript level was seen in the belly flap of fasted fish than in fed fish, even after re-feeding on Day 2. The data do not reveal causative roles of the investigated brain neuropeptides, or leptin, in appetite regulation. It is suggested that the elevated pomc transcript levels provide a satiety signal that reduces energy expenditure during prolonged fasting. The increase in belly flap leptin transcript with fasting, which did not decrease upon re-feeding, indicates a tissue-specific role of leptin in long-term regulation of energy homeostasis.

Dietary contaminant exposure affects plasma testosterone, but not thyroid hormones, vitamin A, and vitamin E, in male juvenile arctic foxes (Vulpes lagopus).

Levels of persistent organic pollutants (POP), such as polychlorinated biphenyls (PCB), are high in many Arctic top predators, including the Arctic fox (Vulpes lagopus). The aim of this study was to examine possible endocrine-disruptive effects of dietary POP exposure in male juvenile Arctic foxes in a controlled exposure experiment. The study was conducted using domesticated farmed blue foxes (Vulpes lagopus) as a model species. Two groups of newly weaned male foxes received a diet supplemented with either minke whale (Baleneoptera acutorostrata) blubber that was naturally contaminated with POP (exposed group, n = 5 or 21), or pork (Sus scrofa) fat (control group, n = 5 or 21). When the foxes were 6 mo old and had received the 2 diets for approximately 4 mo (147 d), effects of the dietary exposure to POP on plasma concentrations of testosterone (T), thyroid hormones (TH), thyroid-stimulating hormone (TSH), retinol (vitamin A), and tocopherol (viramin E) were examined. At sampling, the total body concentrations of 104 PCB congeners were 0.1 ± 0.03 µg/g lipid weight (l.w.; n = 5 [mean ± standard deviation]) and 1.5 ± 0.17 µg/g l.w. (n = 5) in the control and exposed groups, respectively. Plasma testosterone concentrations in the exposed male foxes were significantly lower than in the control males, being approximately 25% of that in the exposed foxes. There were no between-treatment differences for TH, TSH, retinol, or tocopherol. The results suggest that the high POP levels experienced by costal populations of Arctic foxes, such as in Svalbard and Iceland, may result in delayed masculine maturation during adolescence. Sex hormone disruption during puberty may thus have lifetime consequences on all aspects of reproductive function in adult male foxes.

Monitoring contaminants from oil production at sea by measuring gill EROD activity in Atlantic cod (Gadus morhua).

An ex vivo gill EROD assay was applied in Atlantic cod (Gadus morhua) as a biomarker for waterborne CYP1A-inducing compounds derived from oil production at sea. Exposure to nominal concentrations of 1 ppm or 10 ppm North Sea crude oil in a static water system for 24 h caused a concentration-dependent gill EROD induction. Further, exposure of cod for 14 days to environmentally relevant concentrations of produced water (PW, diluted 1:200 or 1:1000) from a platform in the North Sea using a flow-through system resulted in a concentration-dependent induction of gill EROD. Crude oil (0.2 ppm) from the same oil field also proved to induce EROD. Finally, gill EROD activity in cod caged for 6 weeks at 500-10 000 m from two platforms outside Norway was measured. The activities in these fish were very low and did not differ from those in fish caged at reference sites.