4.5 Article

Phosphatidylcholine in Krill Meal and Krill Oil as a Source of Choline for Prevention of Intestinal Steatosis in Atlantic Salmon

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AQUACULTURE RESEARCH
卷 2023, 期 -, 页码 -

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WILEY
DOI: 10.1155/2023/4001633

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Intestinal steatosis, or lipid malabsorption syndrome (LMS), is a common condition in farmed Atlantic salmon, caused by choline deficiency. This study aimed to determine the effectiveness of phosphatidylcholine (PC) from krill meal (KM) and krill oil (KO) in reducing steatosis. Results showed that suboptimal levels of PC from KM and KO were able to promote growth in Atlantic salmon, but a higher PC level was needed to completely eliminate lipid accumulation in the pyloric intestine (PI).
Intestinal steatosis, called lipid malabsorption syndrome (LMS) in severe cases, is a common condition in farmed Atlantic salmon, associated with choline deficiency causing low lipid transport in enterocytes, excessive lipid accumulation, and increased mucosal weight. A previous dose-response study supplying a plant-based diet with choline chloride indicated that 3.4 g/kg choline prevents LMS in Atlantic salmon. However, no similar documentation exists using phosphatidylcholine (PC) as a choline source. The present study therefore aimed to determine the ability of PC from krill meal (KM) and krill oil (KO) towards reducing steatosis in Atlantic salmon. Two diets with suboptimal PC levels (1.5 and 2.6 g/kg) were tested against two control diets, a choline-deficient diet with no supplementation (0.6 g/kg), and a high choline (4.0 g/kg choline chloride) diet. After 8 weeks of freshwater feeding, growth was significantly higher in KM and KO groups, at both PC levels, in comparison to the choline-deficient group. However, growth was significantly higher only in the KM and KO diets with 2.6 g/kg of PC when compared to the positive control. This indicated that suboptimal levels of PC from KM and KO satisfied choline needs for growth. A clear dose-dependent effect on the decreasing pyloric intestine (PI) somatic index was observed for KM and KO diets, with no significant difference between KM and KO diets (2.6 g/kg choline) and high choline reference diet. Accordingly, PC from both KM and KO significantly reduced lipid accumulation in the PI and liver when added to a choline-deficient diet. However, histological and lipid analyses also indicated that the optimal dietary choline requirement for full elimination of lipid accumulation in PI is higher than 2.6 g/kg with KM and KO as supplementary sources.

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