Adiposity and growth of post-smolt Atlantic salmon Salmo salar L.

The long‐term adipose homeostasis seen in mammals gives rise to a ‘lipostatic’ model in which signals produced in proportion to fat stores serve to regulate energy intake. An extension of this predicts an impact of these signals on growth; downregulation of feeding in animals with increased adiposity should result in reduced growth. This was tested by monitoring fat deposition and growth in Atlantic salmon Salmo salar L. provided with feeds that differed in fat content. Salmon parr (mass c. 20 g) were fed either high‐ (H: 34%) or low‐fat (L: 22%) feeds, based on either fish (F) or vegetable (V) oils for 6 months to create groups of fish that differed in adiposity (10–12% and 5–7% body fat) at parr–smolt transformation (mass c. 130 g). Fish fed the high‐fat feeds deposited more body fat, and this was confirmed by measurement of fat concentrations in the fillet, viscera and remaining carcass. The fish were then grown‐on in sea water (c. 35 g L^?1, 8 °C, 24L:0D) for 14 weeks while being fed either high‐ or low‐fat feed formulated with fish oil to give the following treatments: HF→ H, HF→ L, LF→ L, LF→ H, HV→ H, HV→ L, LV→ L, LV→ H. Although fish exposed to the various feed treatments did not differ markedly in growth rate (SGR range 1–1.14% day^?1) over the 14 weeks of rearing in sea water, the results were in general agreement with predictions from the ‘lipostatic’ model, i.e. fish with the greatest fat reserves after the parr–smolt transformation grew more slowly than fish that were ‘leaner’ at this time. This suggests that adiposity, or ‘fatness’, may exert a negative feedback on feeding in salmon, thereby having an influence upon growth.