Foamy, whitish appearance of the pyloric caeca, reflecting elevated lipid content, histologically visible as hypervacuolation, is frequently observed in Atlantic salmon fed high-plant diets. Lipid malabsorption syndrome (LMS) is suggested as term for the phenomenon. Earlier studies have shown that insufficient supply of phospholipids may cause similar symptoms. The objective of the present study was to strengthen knowledge on the role of choline, the key component of phosphatidylcholine, in development of LMS as well as finding the dietary required choline level in Atlantic salmon. A regression design was chosen to be able to estimate the dietary requirement level of choline, if found essential for the prevention of LMS. Atlantic salmon (456 g) were fed diets supplemented with 0, 392, 785, 1177, 1569, 1962, 2354, 2746 and 3139 mg/kg choline chloride. Fish fed the lowest-choline diet had pyloric caeca with whitish foamy surface, elevated relative weight, and the enterocytes were hypervacuolated. These characteristics diminished with increasing choline level and levelled off at levels of 2850, 3593 and 2310 mg/kg, respectively. The concomitant alterations in expression of genes related to phosphatidylcholine synthesis, cholesterol biosynthesis, lipid transport and storage confirmed the importance of choline in lipid turnover in the intestine and ability to prevent LMS. Based on the observations of the present study, the lowest level of choline which prevents LMS and intestinal lipid hypervacuolation in post-smolt Atlantic salmon is 3·4 g/kg. However, the optimal level most likely depends on the feed intake and dietary lipid level.

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Background Various intestinal morphological alterations have been reported in cultured fish fed diets with high contents of plant ingredients. Since 2000, salmon farmers have reported symptoms indicating an intestinal problem, which we suggest calling lipid malabsorption syndrome (LMS), characterized by pale and foamy appearance of the enterocytes of the pyloric caeca, the result of lipid accumulation. The objective of the present study was to investigate if insufficient dietary choline may be a key component in development of the LMS. Results The results showed that Atlantic salmon (Salmo salar), average weight 362 g, fed a plant based diet for 79 days developed signs of LMS. In fish fed a similar diet supplemented with 0.4% choline chloride no signs of LMS were seen. The relative weight of the pyloric caeca was 40% lower, reflecting 65% less triacylglycerol content and histologically normal gut mucosa. Choline supplementation further increased specific fish growth by 18%. The concomitant alterations in intestinal gene expression related to phosphatidylcholine synthesis (chk and pcyt1a), cholesterol transport (abcg5 and npc1l1), lipid metabolism and transport (mgat2a and fabp2) and lipoprotein formation (apoA1 and apoAIV) confirmed the importance of choline in lipid turnover in the intestine and its ability to prevent LMS. Another important observation was the apparent correlation between plin2 expression and degree of enterocyte hyper-vacuolation observed in the current study, which suggests that plin2 may serve as a marker for intestinal lipid accumulation and steatosis in fish. Future research should be conducted to strengthen the knowledge of choline’s critical role in lipid transport, phospholipid synthesis and lipoprotein secretion to improve formulations of plant based diets for larger fish and to prevent LMS. Conclusions Choline prevents excessive lipid accumulation in the proximal intestine and is essential for Atlantic salmon in seawater.

Altered lipid metabolism has been shown in fish fed plant protein sources. The present study aimed to gain further insights into how intestinal and hepatic lipid absorption and metabolism are modulated by plant meal (PM) and soya-saponin (SA) inclusion in salmon feed. Post-smolt Atlantic salmon were fed for 10 weeks one of four diets based on fishmeal or PM, with or without 10 g/kg SA. PM inclusion resulted in decreased growth performance, excessive lipid droplet accumulation in the pyloric caeca and liver, and reduced plasma cholesterol levels. Intestinal and hepatic gene expression profiling revealed an up-regulation of the expression of genes involved in lipid absorption and lipoprotein (LP) synthesis (apo, fatty acid transporters, microsomal TAG transfer protein, acyl-CoA cholesterol acyltransferase, choline kinase and choline-phosphate cytidylyltransferase A), cholesterol synthesis (3-hydroxy-3-methylglutaryl-CoA reductase) and associated transcription factors (sterol regulatory element-binding protein 2 and PPARg). SA inclusion resulted in reduced body pools of cholesterol and bile salts. The hepatic gene expression of the rate-limiting enzyme in bile acid biosynthesis (cytochrome P450 7A1 (cyp7a1)) as well as the transcription factor liver X receptor and the bile acid transporter abcb11 (ATP-binding cassette B11) was down-regulated by SA inclusion. A significant interaction was observed between PM inclusion and SA inclusion for plasma cholesterol levels. In conclusion, gene expression profiling suggested that the capacity for LP assembly and cholesterol synthesis was up-regulated by PM exposure, probably as a compensatory mechanism for excessive lipid droplet accumulation and reduced plasma cholesterol levels. SA inclusion had hypocholesterolaemic effects on Atlantic salmon, accompanied by decreased bile salt metabolism.