Algae in fish feed: performances and fatty acid metabolism in juvenile Atlantic Salmon

Algae are at the base of the aquatic food chain, producing the food resources that fish are adapted to consume. Previous studies have proven that the inclusion of small amounts (<10% of the diet) of algae in fish feed (aquafeed) resulted in positive effects in growth performance and feed utilisation efficiency. Marine algae have also been shown to possess functional activities, helping in the mediation of lipid metabolism, and therefore are increasingly studied in human and animal nutrition. The aim of this study was to assess the potentials of two commercially available algae derived products (dry algae meal), Verdemin (derived from Ulva ohnoi) and Rosamin (derived from diatom Entomoneis spp.) for their possible inclusion into diet of Atlantic Salmon (Salmo salar). Fish performances, feed efficiency, lipid metabolism and final product quality were assessed to investigated the potential of the two algae products (in isolation at two inclusion levels, 2.5% and 5%, or in combination), in experimental diets specifically formulated with low fish meal and fish oil content. The results indicate that inclusion of algae product Verdemin and Rosamin at level of 2.5 and 5.0% did not cause any major positive, nor negative, effect in Atlantic Salmon growth and feed efficiency. An increase in the omega-3 long-chain polyunsaturated fatty acid (n-3 LC-PUFA) content in whole body of fish fed 5% Rosamin was observed

Δ-6 desaturase substrate competition : dietary linoleic acid (18∶2n-6) has only trivial effects on α-linolenic acid (18∶3n-3) bioconversion in the teleost rainbow trout

It is generally accepted that, in vertebrates, omega-3 (n-3) and omega-6 (n-6) poly-unsaturated fatty acids (PUFA) compete for ?-6 desaturase enzyme in order to be bioconverted into long-chain PUFA (LC-PUFA). However, recent studies into teleost fatty acid metabolism suggest that these metabolic processes may not conform entirely to what has been previously observed in mammals and other animal models. Recent work on rainbow trout has led us to question specifically if linoleic acid (LA, 18:2n-6) and ?-linolenic acid (ALA, 18:3n-3) (?-6 desaturase substrates) are in direct competition for access to ?-6 desaturase. Two experimental diets were formulated with fixed levels of ALA, while LA levels were varied (high and low) to examine if increased availability of LA would result in decreased bioconversion of ALA to its LC-PUFA products through substrate competition. No significant difference in ALA metabolism towards n-3 LC-PUFA was exhibited between diets while significant differences were observed in LA metabolism towards n-6 LC-PUFA. These results are evidence for minor if any competition between substrates for ?-6 desaturase, suggesting that, paradoxically, the activity of ?-6 desaturase on n-3 and n-6 substrates is independent. These results call for a paradigm shift in the way we approach teleost fatty acid metabolism. The findings are also important with regard to diet formulation in the aquaculture industry as they indicate that there should be no concern for possible substrate competition between 18:3n-3 and 18:2n-6, when aiming at increased n-3 LC-PUFA bioconversion in vivo

Metabolic fate (absorption, β-oxidation and deposition) of long-chain n-3 fatty acids is affected by sex and by the oil source (krill oil or fish oil) in the rat

The effects of krill oil as an alternative source of n-3 long-chain PUFA have been investigated recently. There are conflicting results from the few available studies comparing fish oil and krill oil. The aim of this study was to compare the bioavailability and metabolic fate (absorption, β-oxidation and tissue deposition) of n-3 fatty acids originating from krill oil (phospholipid-rich) or fish oil (TAG-rich) in rats of both sexes using the whole-body fatty acid balance method. Sprague-Dawley rats (thirty-six male, thirty-six female) were randomly assigned to be fed either a krill oil diet (EPA+DHA+DPA=1·38 mg/g of diet) or a fish oil diet (EPA+DHA+DPA=1·61 mg/g of diet) to constant ration for 6 weeks. The faeces, whole body and individual tissues were analysed for fatty acid content. Absorption of fatty acids was significantly greater in female rats and was only minimally affected by the oil type. It was estimated that most of EPA (>90 %) and more than half of DHA (>60 %) were β-oxidised in both diet groups. Most of the DPA was β-oxidised (57 and 67 % for female and male rats, respectively) in the fish oil group; however, for the krill oil group, the majority of DPA was deposited (82-83 %). There was a significantly greater deposition of DPA and DHA in rats fed krill oil compared with those fed fish oil, not due to a difference in bioavailability (absorption) but rather due to a difference in metabolic fate (anabolism v. catabolism)

Targeted dietary micronutrient fortification modulates n-3 LC-PUFA pathway activity in rainbow trout (Oncorhynchus mykiss)

Replacing fish oil (FO) in aquafeeds with sustainable alternatives such as vegetable oils (VO) compromises the content of n-3 long-chain polyunsaturated fatty acid (n-3 LC-PUFA) in the edible portions of farmed fish. Endogenous biosynthesis of n-3 LC-PUFA from C18 precursors is catalysed by several enzymes, which have low activity in carnivorous fish. Rainbow trout were fed on VO-based diets supplemented with increasing levels of selected micronutrients as potential n-3 LC-PUFA biosynthesis co-factors or coenzyme precursors: iron, zinc, magnesium, niacin, riboflavin, pyridoxine and biotin at 100, 200, 300 or 400% of their recommended dietary inclusion. Providing the substrate (ALA, 18:3n-3) and the potential enzyme co-factors was assumed to enhance the efficiency of EPA (20:5n-3) and DHA (22:6n-3) production. Initial evidence was established when DHA and total n-3 LC-PUFA content increased in the whole body of fish from the treatment with the highest micronutrient fortification. Fewer changes were observed in the fillet or liver which was consistent with a marginal regulation of the mRNA expression of key biosynthesis genes in the liver. The potential co-factors seem to stimulate the n-3 LC-PUFA biosynthesis efficiency at the molecular and enzymatic level in rainbow trout fed on ALA-rich diet, leading to metabolic and chemical changes. The interactions between dietary substrate and enzyme co-factors/coenzymes need to be further investigated to advance lipid metabolism research and benefit the aquaculture industry. © 2013 Elsevier B.V

The apparent <i>in vivo</i> fate of 18∶2n-6 or 18∶3n-3 towards direct elongation to 20∶2n-6 or 20∶3n-3, Δ-6 desaturation to 18∶3n-6 or 18∶4n-3, β-oxidation or deposition as is, expressed as percentage of dietary net intake, in rainbow trout fed the two experimental diets (LLA and HLA) and deduced by the whole-body fatty acid balance method.

<p>(<b>A</b>) <i>in vivo</i> fate of 18∶2n-6 in trout fed LLA; (<b>B</b>) <i>in vivo</i> fate of 18∶2n-6 in trout fed HLA; (<b>C</b>) <i>in vivo</i> fate of 18∶3n-3 in trout fed LLA; (<b>D</b>) <i>in vivo</i> fate of 18∶3n-3 in trout fed HLA. In each graph, data represent mean values (<i>n</i>  = 3; <i>N</i>  = 6), and the only statistically significant difference recorded was for the percentage of 18∶3n-3 directly elongated to 18∶4n-3 in trout fed LLA or HLA (*P<0.05).</p

Formulation and proximate composition of the experimental diets.

1<p>Experimental diets abbreviations: LLA Low Linoleic Acid diet; HLA – High Linoleic Acid diet.</p>2<p>Basal diet composition (g/kg): fish meal 129.4; poultry by-product meal 318.5; soybean protein concentrate 124.4; blood meal 24.9; pre-gelatinised starch 209.0; mineral and vitamin mix 8; amino acid mix (methionine, lysine, aspartic acid and glutamic acid) 23.6; Celite® 5.</p>3<p>Nitrogen free extracts calculated by difference.</p>4<p>Calculated on the basis of 23.6, 39.5 and 17.2 kJ/g of protein, fat and carbohydrate, respectively.</p

The apparent <i>in vivo</i> 18∶2n-6 and 18∶3n-3 bioconversion activity (nmol/g/day) in rainbow trout fed the two experimental diets (LLA and HLA) and deduced by the whole-body fatty acid balance method.

<p>Graphs are reported following the PUFA bioconversion pathway, from (<b>A</b>) substrate availability (dietary net intake); towards i) the dead end pathway (on the left): (<b>B</b>) elongation of 18∶2n-6 and 18∶3n-3; (<b>C</b>) elongation of 20∶2n-6 and 20∶3n-3; and ii) the LC-PUFA biosynthetic pathway(on the right): (<b>D</b>) Δ-6 desaturation of 18∶2n-6 and 18∶3n-3; (<b>E</b>) Elongation of 18∶3n-6 and 18∶4n-3; (<b>F</b>) Δ-5 desaturation of 20∶3n-6 and 20∶4n-3; (<b>G</b>) Elongation of 20∶4n-6 and 20∶5n-3; (<b>G</b>) Elongation, Δ-6 desaturation and chain shortening of 22∶4n-6 and 22∶5n-3. In each graph, bars represent mean ± s.e.m., <i>n</i>  = 3; <i>N</i>  = 6. P-value: <i>ns</i> = not significant; *, ** and *** indicate P<0.05, <0.01 and <0.001, respectively.</p

Formulation and proximate composition of the two experimental diets with (H-Chol) or without (L-Chol) cholesterol fortification.

1<p>Experimental diet nomenclature: L-Chol diet contained no added cholesterol, H-Chol diet containing 1 g Kg⁻¹. added cholesterol.</p>2<p>Basal diet composition (g Kg⁻¹): poultry meal 211, soy protein concentrate 144, fish meal 87, blood meal 66, soybean meal 58, wheat gluten 57, whey protein 40; Ridley Agriproducts, Narangba, Queensland, Australia.</p>3<p>Vegetable oil: 70% linseed oil, Sceney Chemical Pty., Ltd., Sunshine, VIC, Australia and 30% Canola oil, Black and Gold, Tooronga, VIC. Australia.</p>4<p>Starch: Pre-gel starch, Ridley Agriproducts, Narangba, Queensland, Australia.</p>5<p>Min & Vit.: Complete minerals and vitamins mix supplement; Sigma-Aldrich, Inc. St. Louis, MO, USA.</p>6<p>Others (g Kg⁻¹): Amino acid mix (L-Methionine, L-Lysine, glutamic acid) 3, Celite® 7, Sigma-Aldrich, Inc. St. Louis, MO, USA.</p>7<p>a-cellulose: alpha cellulose, Sigma-Aldrich, Inc. St. Louis, MO, USA.</p>8<p>Cholesterol: Sigma-Aldrich, Inc. St. Louis, MO, USA.</p>9<p>NFE: Nitrogen free extract calculated by difference.</p>10<p>Calculated on the basis of 23.6, 39.5 and 17.2 KJ g⁻¹ of protein, fat and carbohydrate, respectively.</p