Dietary calcifediol reduces mesenteric adiposity to the benefit of carcass growth independently of circulating vitamin D hormone in juvenile Atlantic salmon
Dietary calcifediol reduces mesenteric adiposity to the benefit of carcass growth independently of circulating vitamin D hormone in juvenile Atlantic salmon
Authors
Rider, S.
Yamashita, E.
Chenal, E.
Cabo Valcarce, P.
Kuschel, F.
Orellana, P.
Ruiz, J.
Hernandez, A.
Dantagnan, P.
Yamashita, E.
Chenal, E.
Cabo Valcarce, P.
Kuschel, F.
Orellana, P.
Ruiz, J.
Hernandez, A.
Dantagnan, P.
Profesor GuĆa
Authors
Date
Datos de publicaciĆ³n:
10.1016/j.aquaculture.2024.740687
AQUACULTURE,Vol.585,2024
AQUACULTURE,Vol.585,2024
Tipo de recurso
Article
Keywords
Materia geogrƔfica
Collections
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.