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Tryptophan (Trp) is an essential amino acid, commercially available as a feed-grade product, and is a precursor to serotonin and melatonin, which are both important molecules in stress mitigation. Meagre have a high potential for marine aquaculture diversification but are highly susceptible to stressful conditions. This study aimed to assess the potential role of dietary tryptophan supplementation in meagre juveniles in order to minimize the deleterious effect of potential stress conditions. For this, a growth trial was performed wherein meagre juveniles were fed four isoproteic (45%DM) and isolipidic (16%DM) diets; namely, a control diet, and three diets similar to the control diet but supplemented with varying levels of tryptophan, graded according to the resulting percentage in each diet's dry matter (Control, 0.25%Trp, 0.5%Trp, and 1%Trp), corresponding to a total dietary tryptophan of 1.06, 1.70, 2.08, and 3.24 g 16 g−1 N, respectively. Diets were tested in triplicate, and fish were fed twice a day, six days a week, for eight weeks. Five days after the end of the growth trial, a time-course blood sampling was performed at 0 h, 1 h, 3 h, 6 h, and 12 h after feeding. At the 6 h sampling point, the liver was also collected. Overall, our results indicate that 1Trp supplementation (total dietary Trp 3.24 g 16 g−1 N) may be harmful to fish, decreasing growth performance and feed utilization, although doses up to 0.5Trp do not influence these parameters. Voluntary feed intake lineally decreased with the increase in the level of dietary Trp. Whole-body lipid content decreased at the highest tryptophan inclusion, whereas no changes were observed in protein levels. After 12 h from feeding, plasma glucose levels were lower in all dietary treatments supplemented with tryptophan compared to those observed in the control. Hepatic enzyme activity of protein catabolism decreased with dietary Trp inclusion. Overall, our results suggested that while a dietary Trp level increase of up to 2.08 g 16 g−1 N did not affect growth performance and feed efficiency, both these parameters were severely compromised with a Trp level of 3.24 g 16 g−1 N. [ABSTRACT FROM AUTHOR]

Tryptophan (Trp) is an essential amino acid, commercially available as a feed-grade product, and is a precursor to serotonin and melatonin, which are both important molecules in stress mitigation. Meagre have a high potential for marine aquaculture diversification but are highly susceptible to stressful conditions. This study aimed to assess the potential role of dietary tryptophan supplementation in meagre juveniles in order to minimize the deleterious effect of potential stress conditions. For this, a growth trial was performed wherein meagre juveniles were fed four isoproteic (45%DM) and isolipidic (16%DM) diets; namely, a control diet, and three diets similar to the control diet but supplemented with varying levels of tryptophan, graded according to the resulting percentage in each diet’s dry matter (Control, 0.25%Trp, 0.5%Trp, and 1%Trp), corresponding to a total dietary tryptophan of 1.06, 1.70, 2.08, and 3.24 g 16 g−1 N, respectively. Diets were tested in triplicate, and fish were fed twice a day, six days a week, for eight weeks. Five days after the end of the growth trial, a time-course blood sampling was performed at 0 h, 1 h, 3 h, 6 h, and 12 h after feeding. At the 6 h sampling point, the liver was also collected. Overall, our results indicate that 1Trp supplementation (total dietary Trp 3.24 g 16 g−1 N) may be harmful to fish, decreasing growth performance and feed utilization, although doses up to 0.5Trp do not influence these parameters. Voluntary feed intake lineally decreased with the increase in the level of dietary Trp. Whole-body lipid content decreased at the highest tryptophan inclusion, whereas no changes were observed in protein levels. After 12 h from feeding, plasma glucose levels were lower in all dietary treatments supplemented with tryptophan compared to those observed in the control. Hepatic enzyme activity of protein catabolism decreased with dietary Trp inclusion. Overall, our results suggested that while a dietary Trp level increase of up to 2.08 g 16 g−1 N did not affect growth performance and feed efficiency, both these parameters were severely compromised with a Trp level of 3.24 g 16 g−1 N.

This study aimed at assessing the effects of the dietary tryptophan (Trp) supplementation on growth and feed utilization, brain serotonin content, and expression of selected liver genes (involved in the liver serotonin pathway, protein synthesis degradation, and antioxidant activity) in zebrafish. A growth trial was conducted with zebrafish juveniles fed five experimental isoproteic (40%DM) and isolipidic (8%DM) fishmeal-based diets containing graded levels of Trp: a Trp-non-supplemented diet (diet Trp0, with 0.22% Trp) and four Trp-supplemented diets containing 2–16 times higher Trp content (diets Trp2, Trp4, Trp8, and Trp16 with 0.40, 0.91, 2.02, and 3.34% Trp, respectively). Diets were tested in quadruplicate, with fish being fed twice a day, 6 days a week for 6 weeks to apparent visual satiation. At the end of the trial, growth performance and feed utilization were assessed, and fish from all experimental groups were sampled for whole-body composition analysis. In addition, fish fed low (Trp0), medium (Trp4), and high (Trp16) Trp diets were also sampled for analysis of brain serotonin content and liver gene expression. Tested tryptophan levels did not influence growth performance nor feed intake. However, values of energy and nitrogen retention as well as body energy content indicate a better feed utilization with diets containing around 0.9% and 2.0% DM Trp. Brain serotonin content increased with increasing dietary tryptophan levels. In addition, regarding liver genes, dietary treatment had a modulatory effect on the expression of Htr1aa and Htr2cl1 genes (encoding for serotonin receptors), TPH1a gene (encoding for tryptophan hydroxylase, the rate-limiting enzyme in the synthesis of serotonin from tryptophan), TOR gene (involved in protein synthesis), and Keap1 gene (involved in antioxidant responses). [ABSTRACT FROM AUTHOR]