4.5 Article

The replacement of fish meal with Antarctic krill, Euphausia superba in diets for Atlantic salmon, Salmo salar

期刊

AQUACULTURE NUTRITION
卷 12, 期 4, 页码 280-290

出版社

WILEY
DOI: 10.1111/j.1365-2095.2006.00400.x

关键词

chitin; digestibility; fatty acid composition; feed utilization; growth rate; krill

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A total of six isoprotein and isolipid diets for Atlantic salmon, Salmo salar L., were prepared substituting from 0 to 100% of fish meal protein (0-68% of diet by dry weight) with meal from Antarctic krill (Euphausia superba). The feed produced from high inclusion levels of krill meal had lower ability to absorb lipid during vacuum coating than fish meal. Both amino acid and fatty acid compositions of the diets were fairly similar. The experiment commenced using salmon averaging 500 g and ended at a mean weight of 1500-1800 g (140 days of feeding). Moderate amounts of krill meal (20-60% of krill protein) in the diets increased growth during the first 71 days of feeding compared with the fish meal control, while no growth difference was observed during the last 69 days of feeding. This may, at least in parts, be explained by a feed-attractant function of the krill meal. Muscle dry weight and lipid concentrations were unaffected by the diet. Feed conversion rate increased with high levels of krill meal in the diets (e. g. for the last period from 0.94 in the 0% diet to 1.26 in the 100% diet). This indicates that the fish were able to compensate by eating more to maintain growth. The apparent digestibility coefficients of dry matter and protein were not influenced by diet, but both faecal moisture and lipid had a tendency to increase at the highest inclusion level (all protein from krill meal). This may be related to chitin in the krill diet that is known to decrease lipid absorption and induce diarrhoea (increased water content in faeces). Chitin was not utilized to any major extent. Welfare parameters such as blood haemoglobin, red blood cell counts, plasma protein, cholesterol, triacylglycerols and glucose levels were unaffected by diets. Clinical indicators of cellular damage (alanine aminotransferase and aspartate aminotransferase) were similar indicating no diet-induced tissue damage during the trial.

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