Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/76358
Campo DC Valoridioma
dc.contributor.authorAlami-Durante, Hélèneen_US
dc.contributor.authorBazin, Didieren_US
dc.contributor.authorCluzeaud, Marianneen_US
dc.contributor.authorFontagné-Dicharry, Stéphanieen_US
dc.contributor.authorKaushik, Sadasivamen_US
dc.contributor.authorGeurden, Ingeen_US
dc.date.accessioned2020-12-04T14:06:45Z-
dc.date.available2020-12-04T14:06:45Z-
dc.date.issued2018en_US
dc.identifier.issn0044-8486en_US
dc.identifier.urihttp://hdl.handle.net/10553/76358-
dc.description.abstractThe aim of the study was to analyse the effects of different dietary methionine (Met) concentrations on themechanisms offish muscle growth (hyperplasia and hypertrophy) by using cellular and molecular approaches.Three plant-based diets differing by their Met level (MD, Met-deficient; MC, Met-control, corresponding to es-tablished Met requirement; MH, Met-high) were fed to rainbow trout juveniles for 12 weeks. Met deficiency ledto a reduced somatic growth right from thefirst 3 weeks of feeding onwards, while feeding the MH-diet led to anincreased body growth in the 6 last weeks of feeding. The protein gain of the juveniles increased with dietaryMet content. The protein retention efficiency of the MD-fed juveniles was half that of the MC- and MH-fedjuveniles which were statistically similar. The changes induced by MD- and MH-feeding at muscle molecular andcellular levels were different. Compared to control, dietary Met deficiency altered the expression of myogenic,muscle growth- and metabolism-related genes by increasing Myf5, MyoD1, Mrf4, Mef2a,βact, CathD, GSTπandTNFαexpressions and decreasing Col1α1 and IGF1 expressions, whereas a high level of dietary Met decreasedPax7a2, Mef2c,βact, CathD, GDH2 and NF-κB expressions. The Met-control fedfish were discrimated accordingto HGF, Pax7a1 and Pax7a2 expressions. Dietary Met level thus acted on the expression of genes regulatingspecific transition points of myogenesis, and affected the expression of muscle structural genes and growthfactors involved in satellite cell activation and muscle growth. Molecular results suggested that MD-diet favourssatellite cell return to quiescence, while MC-diet favours satellite cell activation and MH-diet myogenic differ-entiation. At cellular level, the muscle total cross-sectional area of the juveniles fed the MD-diet was 28% lowerthan that of the juveniles fed the MC-diet despite a similar total number of white musclefibres, and the numberof white musclefibres with a large diameter was lower in MD-fedfish than in MC-fed ones. The muscle totalcross-sectional area of the juveniles fed the MH-diet was 32% higher than that of the juveniles fed the MC-diet,their total number of white musclefibres 25% higher, and their number of white musclefibres with a largediameter similar. Increasing dietary methionine above established requirement thus promotes white musclehyperplasia and muscle growth in rainbow trout juveniles, while methionine deficiency dysregulates the ex-pression of myogenic and muscle growth-related genes and impairs whitefibre hypertrophy.Statement of relevance:Determining the effects of dietary methionine levels on muscle growth mechanisms willhelp develop lowfish meal feeds.en_US
dc.languageengen_US
dc.relationAdvanced Research Initiatives For Nutrition & Aquacultureen_US
dc.relation.ispartofAquacultureen_US
dc.sourceAquaculture [ISSN 0044-8486], v. 483, p. 273-285en_US
dc.subject310502 Pisciculturaen_US
dc.subject.otherNutritionen_US
dc.subject.otherMethionineen_US
dc.subject.otherMuscle growthen_US
dc.subject.otherHyperplasiaen_US
dc.subject.otherGene expressionen_US
dc.subject.otherCellularityen_US
dc.titleEffect of dietary methionine level on muscle growth mechanisms in juvenile rainbow trout ( Oncorhynchus mykiss )en_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.aquaculture.2017.10.030en_US
dc.description.lastpage285en_US
dc.description.firstpage273en_US
dc.relation.volume283en_US
dc.investigacionCienciasen_US
dc.type2Artículoen_US
dc.description.numberofpages13en_US
dc.date.coverdateEnero 2018en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-BASen_US
dc.description.sjr1,154
dc.description.jcr3,022
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.project.principalinvestigatorIzquierdo López, María Soledad-
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