Weight gain and lipid deposition in Atlantic salmon, Salmo salar , during compensatory growth: evidence for lipostatic regulation?

Abstract

Feed-restricted fish gain less body mass and storage reserves than well-fed fish, and reduced rates of gain often trigger compensatory responses, characterized by increased appetite (hyperphagia) and growth rate. The results of previous investigations have introduced a hypothesis in which adipose tissue (fat stores) had a regulatory role in governing appetite. An extension of this suggests that hyperphagia may relate to the severity of the feed restriction, and that the compensatory responses will cease once fat reserves are restored relative to body size. This was tested in two trials in which feed-restricted or -deprived postsmolt Atlantic salmon, Salmo salar, became hyperphagic after transfer to excess feeding. At the end of the first trial, previously feed-restricted fish had fully compensated for their lost weight gain compared to continuously fed control fish, but had a leaner body composition (i.e. reduced energy stores) and were still showing signs of compensatory growth. In the second trial, feed deprivation drained body lipids and caused a stronger hyperphagic response than restrictive feeding, although it took longer to develop. Feed intake became coincident when fish had a similar body composition for size, but this occurred at different times. Hence, the fish that had been deprived of feed were smaller than the restricted fish at the end of the trial. The results of the present study demonstrate a link between the magnitude of lipid stores, feed intake and weight gain, and provide some evidence for lipostatic appetite regulation in fish.