Abstract

Dietary vitamin D is required by cultivated fish for optimal growth, feed utilisation and bone health. The in vivo conversion of cholecalciferol (D3) to active vitamin D hormone (1,25-OH-D3) may be impaired in farm-raised fish fed modern feed formulations. Requiring fewer metabolic steps for its conversion, the use of dietary calcifediol (25-OH-D3) may mitigate against deficits in vitamin D metabolism. A 90-day experimental feeding trial was undertaken in juvenile (23 g) Atlantic salmon (Salmo salar) to test the efficacy of 25-OH-D3 added to a standard diet containing recommended levels of D3 (5640 IU). Test diets contained 100, 200 or 400 mu g/kg added 25-OH-D3 against a no additive control diet. Effects on zootechnical performance, indices of adiposity, bone mineralisation, and circulating vitamin D metabolites were tested. Dietary 25-OH-D3 significantly reduced feed conversion ratio (FCR) and resulted in numerical increases in growth performance. 25-OH-D3 also significantly reduced mesenteric adiposity with concurrent increases in carcass weight. Levels of calcium, phosphorous, magnesium, zinc and manganese were not modulated in the vertebrae of fish receiving 25-OH-D3. Circulating 25-OH-D3 remained below detection limits and 1,25-OH-D3 was not significantly modulated by the dietary manipulations. The significant reduction of mesenteric adiposity to the benefit of carcass weight shows that dietary 25-OH-D3 improves the utilisation of lipids. The vitamin D requirement for bone mineralisation was met by the basal diet. Segmented regression estimates a dietary 25-OH-D3 supplementation of 143 to 180 mu g/kg for improved feed conversion and reduced mesenteric adiposity. The lack of correlation between circulating vitamin D hormone and mesenteric adiposity indicates that lipid metabolism is regulated by localised tissue activation of vitamin D, rather than the endocrine functions of circulating 1,25-OH-D3.