Parental and early-feeding effects of dietary methionine in rainbow trout (Oncorhynchus mykiss)

We studied the effect of changes in dietary methionine (Met) supply in broodstock and first-feeding rainbow trout fry (offspring). Three plant-based diets differing in Met level (deficient, adequate or in excess of the established requirement) were fed to the broodstock (male and female) for 6 months prior to spawning (diets BD, BA and BE, respectively). The offspring from the parental Met-groups was then challenged in turn with the different Met fry-diets (FD, FA and FE, respectively) for 3 weeks from first-feeding. At spawning, females fed diet BD had significantly higher plasma total and LDL-cholesterol and slightly lower plasma triacylglycerol. Diet BD reduced female (but not male) growth, weight of spawn and egg size, but had no effect on relative fecundity. The free amino acid profile of oocytes was modified, with levels of Met and Cys correlating positively with the Met-levels of broodstock diets. SAM and SAH levels in oocytes followed the same pattern, as opposed to SAM/SAH ratio. At the swim-up stage, no significant effect of parental diet on fry weight was noted, whereas survival was the highest in fry from BE-broodstock. The subsequent 21-day fry feeding with different Met levels highly affected the daily growth index with a significant interaction between the parental-diet and fry-diet effects. The expression of a number of genes regulating sulfur amino acid metabolism was modified either directly by the dietary Met supply in both broodstock liver and in whole fry (e.g. BHMT1, GR, GST pi, MsrA1) or indirectly by the parental Met intakes as seen in the swim-up fry (e.g. BHMT1, MTR, GST pi, MsrA1). Importantly, long-lasting parental effects linked to broodstock Met-intake were seen in the fry, 21-days after first-feeding and irrespective of the fry diet (CTH, MsrA1, MsrB2, SOD2). Similarly, parental effects were noted on the gene expression of both NPY and POMC feeding peptides in fry prior to exogenous feeding which persisted for POMC in the 21-day fry. Parental effects were also demonstrated on the key myogenic gene Myog, on fMHC and GDH in swim-up fry, which persisted for GDH in 21-day fry. In summary, our results demonstrate that dietary Met levels of rainbow trout broodstock affect various traits in the offspring, some of which persisted during the first weeks of exogenous feeding. Further studies need to evaluate the long-term persistence of the parental effects over time and to elucidate the mechanisms, whether epigenetic or not. Statement of relevance: Determining the multiple effects of dietary methionine levels on reproductive, growth performance and metabolism in offspring will help improve formulations of low fish meal feeds for rainbow trout at sensitive life cycle stages. (C) 2016 Elsevier B.V. All rights reserved.EU [288925]F.C.T., Portugal - Fundo Social Europeu (POCH) and National Funds [SFRH/BPD/108389/2015]info:eu-repo/semantics/publishedVersio

Parental Effects of Changes in Dietary Methionine Supply in Rainbow Trout

International audienc

Effect of Dietary Methionine Level on Muscle Growth Mechanisms in Juvenile Rainbow Trout (Oncorhynchus Mykiss)

International audienc

Influence of dietary astaxanthin on the oxidative stress response caused by episodic hyperoxia in rainbow trout

Session Nutrition: Functional AquafeedsInfluence of dietary astaxanthin on the oxidative stress response caused by episodic hyperoxia in rainbow trout. Aquaculture Europe 201

Dietary Methionine Levels under and above Known Requirement Differently Regulate the Muscle Growth Mechanisms of Rainbow Trout (Oncorhynchus Mykiss) Juveniles

poste

Influence of the forms and levels of dietary selenium on antioxidant status and oxidative stress-related parameters in rainbow trout (Oncorhynchus mykiss) fry

Se is an essential micronutrient required for normal growth, development and antioxidant defence. The objective of the present study was to assess the impact of dietary Se sources and levels on the antioxidant status of rainbow trout (Oncorhynchus mykiss) fry. First-feeding fry (initial body weight: 91 mg) were fed either a plant- or fishmeal-based diet containing 0.5 or 1.2mg Se/kg diet supplemented or not with 0.3mg Se/kg diet supplied as Se-enriched yeast or sodium selenite for 12 weeks at 17 degrees C. Growth and survival of rainbow trout fry were not significantly affected by dietary Se sources and levels. Whole-body Se was raised by both Se sources and to a greater extent by Se-yeast. The reduced: oxidised glutathione ratio was raised by Se-yeast, whereas other lipid peroxidation markers were not affected by dietary Se. Whole-body Se-dependent glutathione peroxidase (GPX) activity was enhanced in fish fed Se-yeast compared to fish fed sodium selenite or non-supplemented diets. Activity and gene expression of this enzyme as well as gene expression of selenoprotein P (SelP) were reduced in fish fed the non-supplemented plant- based diet. Catalase, glutamate-cysteine ligase and nuclear factor-erythroid 2-related factor 2 (Nrf2) gene expressions were reduced by Se-yeast. These results suggest the necessity to supplement plant- based diets with Se for rainbow trout fry, and highlight the superiority of organic form of Se to fulfil the dietary Se requirement and sustain the antioxidant status of fish. GPX and SelP expression proved to be good markers of Se status in fish

Impact of Dietary Sulphur Amino Acid Deficiency on Growth Performance, Lipid Peroxidation and Antioxidant Status of Rainbow Trout Fed Diets with Different Protein Levels

International audienc

Influence of dietary astaxanthin on the hepatic oxidative stress response caused by episodic hyperoxia in rainbow trout

A 13-week feeding trial was carried out with juvenile rainbow trout to test two diets: a control diet without astaxanthin (AX) supplementation (CTRL diet), and a diet supplemented with 100 mg/kg of synthetic AX (ASTA diet). During the last week of the feeding trial, fish were exposed to episodic hyperoxia challenge for 8 consecutive hours per day. Episodic hyperoxia induced physiological stress responses characterized by a significant increase in plasma cortisol and hepatic glycogen and a decrease in plasma glucose levels. The decrease of plasma glucose and the increase of hepatic glycogen content due to episodic hyperoxia were emphasized with the ASTA diet. Hyperoxia led to an increase in thiobarbituric acid-reactive substances in the muscle, diminished by dietary AX supplementation in both liver and muscle. Muscle and liver AX were increased and decreased respectively after 7-day episodic hyperoxia, leading to an increase in flesh redness. This augment of muscle AX could not be attributed to AX mobilization, since plasma AX was not affected by hyperoxia. Moreover, hyperoxia decreased most of antioxidant enzyme activities in liver, whereas dietary AX supplementation specifically increased glutathione reductase activity. A higher mRNA level of hepatic glutathione reductase, thioredoxin reductase, and glutamate-cysteine ligase in trout fed the ASTA diet suggests the role of AX in glutathione and thioredoxin recycling and in de novo glutathione synthesis. Indeed, dietary AX supplementation improved the ratio between reduced and oxidized glutathione (GSH/GSSG) in liver. In addition, the ASTA diet up-regulated glucokinase and glucose-6-phosphate dehydrogenase mRNA level in the liver, signaling that dietary AX supplementation may also stimulate the oxidative phase of the pentose phosphate pathway that produces NADPH, which provides reducing power that counteracts oxidative stress. The present results provide a broader understanding of the mechanisms by which dietary AX is involved in the reduction of oxidative statu

Dietary methionine deficiency affects oxidative status, mitochondrial integrity and mitophagy in the liver of rainbow trout (Oncorhynchus mykiss)

The low levels of methionine in vegetable raw materials represent a limit to their use in aquafeed. Methionine is considered as an important factor in the control of oxidative status. However, restriction of dietary methionine has been shown to reduce generation of mitochondrial oxygen radicals and thus oxidative damage in liver. Here, we aim to evaluate the effect of dietary methionine deficiency in hepatic oxidative status in rainbow trout and identify the underlying mechanisms. Fish were fed for 6 weeks diets containing two different methionine concentrations: deficient (MD, Methionine Deficient diet) or adequate (CTL, control diet). At the end of the experiment, fish fed the MD diet showed a significantly lower body weight and feed efficiency compared to fish fed the CTL diet. Growth reduction of the MD group was associated to a general mitochondrial defect and a concomitant decrease of the oxidative status in the liver. The obtained results also revealed a sharp increase of mitochondrial degradation through mitophagy in these conditions and emphasized the involvement of the PINK1/PARKIN axis in this event. Collectively, these results provide a broader understanding of the mechanisms at play in the reduction of oxidant status upon dietary methionine deficiency