Summary
The life-strategy of the anadromous Arctic charr (Salvelinus alpinus) includes several months of voluntary fasting during overwintering in fresh water leading to emaciation prior to seawater migration in spring. In this study we compared changes in condition, substrate utilization and liver metabolism between captive anadromous charr subjected to food-deprivation during late winter and spring, and conspecifics fed in excess. In March, 9 out of the 10 sampled fed fish had not eaten, indicating that they were a voluntary anorexic state. In June, the fed fish were eating and all had higher body mass (BM), condition factor (CF) and adiposity than in March. In fasted fish there were only small decreases in BM, CF and adiposity between March and May, but all these parameters decreased markedly from May to June. The fasted fish were fat- and glycogen-depleted in June, had suppressed activity of hepatic enzymes involved in lipid metabolism (G6PDH and HOAD) and seemed to rely on protein-derived glucose as a major energy source. This was associated with up-regulated liver gene expression of leptin A1, leptin A2, SOCS1, SOCS2 and SOCS3, and reduced IGF-I expression. In an in vitro study with liver slices it was shown that recombinant rainbow trout leptin stimulated SOCS1 and SOCS3 expression, but not SOCS2, IGF-I or genes of enzymes involved in lipid (G6PDH) and amino acid (AspAT) metabolism. It is concluded that liver leptin interacts with SOCS in a paracrine fashion to suppress lipolytic pathways and depress metabolism when fat stores are depleted.
