Dietary calcifediol reduces mesenteric adiposity to the benefit of carcass growth independently of circulating vitamin D hormone in juvenile Atlantic salmon

生物 内分泌学 少年 内科学 钙二醇 维生素D与神经学 生长激素 维生素 激素 维生素D缺乏 生态学 医学
作者
S. Rider,ER. YAMASHITA,E. Chenal,P. Cabo-Valcarce,F. Kuschel,Paola Orellana,Juan Carlos Ruiz,Adrián J. Hernández,Patricio Dantagnan
出处
期刊:Aquaculture [Elsevier BV]
卷期号:585: 740687-740687 被引量:5
标识
DOI:10.1016/j.aquaculture.2024.740687
摘要

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 μg/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 μg/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.
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