Seasonal appetite regulation in the anadromous Arctic charr: Evidence for a role of adiposity in the regulation of appetite but not for leptin in signalling adiposity

The aim of this study was to investigate whether the seasonal feeding cycle of the anadromous Arctic charr (Salvelinus alpinus) is regulated by a lipostatic mechanism and if leptin (Lep) might act as an endocrine signal of adiposity. Offspring of anadromous Arctic charr with a body mass of 121 g were divided into two treatment groups; one was given feed in excess from March to November, and the other was fasted between April and early June and fed in excess thereafter. In the continuously fed group there was an 8-fold increase in body mass, and a doubling of percentage body fat, from March to August, after which there was no further increase. Fish in the other group lost weight and body fat during fasting, but grew rapidly on being fed, and had partially compensated for their deficit in body mass by August. Differences in percentage body fat between treatment groups were eliminated by August, providing evidence for a lipostatic regulation of feeding and energy homeostasis in Arctic charr. Neither liver total LepA gene expression nor plasma Lep concentrations correlated positively with fish adiposity, so there was no evidence that Lep acts as a signal of adiposity in this species. On the other hand, there was a strong increase in liver LepA1 gene expression at the end of the fasting period, concomitant with fat mobilization and increased plasma glucose, indicating that LepA1 may play a role in regulating metabolic processes associated with fasting.

► An 8-fold increase in body mass from April to August. ► Appetite cessation when body fat was restored, indicating a lipostatic regulation. ► No seasonal change in plasma leptin levels. ► No evidence for a adiposity signaling role of leptin. ► An 11-fold increase in liver leptinA1 mRNA expression with long term fasting.