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.