High-fat diet suppresses the positive effect of creatine supplementation on skeletal muscle function by reducing protein expression of IGF-PI3K-AKT-mTOR pathway

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dc.contributor.authorFerretti, Renato [UNESP]
dc.contributor.authorMoura, Eliezer Guimaraes
dc.contributor.authorSantos, Veridiana Carvalho dos [UNESP]
dc.contributor.authorCaldeira, Eduardo Jose
dc.contributor.authorConte, Marcelo
dc.contributor.authorMatsumura, Cintia Yuri [UNESP]
dc.contributor.authorPertille, Adriana
dc.contributor.authorMosqueira, Matias
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionCtr Univ Adventista Sao Paulo
dc.contributor.institutionFMJ
dc.contributor.institutionESEF
dc.contributor.institutionUniv Metodista Piracicaba
dc.contributor.institutionHeidelberg Univ Hosp
dc.date.accessioned2019-10-04T12:31:00Z
dc.date.available2019-10-04T12:31:00Z
dc.date.issued2018-10-04
dc.description.abstractHigh-fat (HF) diets in combination with sedentary lifestyle represent one of the major public health concerns predisposing to obesity and diabetes leading to skeletal muscle atrophy, decreased fiber diameter and muscle mass with accumulation of fat tissue resulting in loss of muscle strength. One strategy to overcome the maleficent effects of HF diet is resistance training, a strategy used to improve muscle mass, reverting the negative effects on obesity-related changes in skeletal muscle. Together with resistance training, supplementation with creatine monohydrate (CrM) in the diet has been used to improve muscle mass and strength. Creatine is a non-essential amino acid that is directly involved in the cross-bridge cycle providing a phosphate group to ADP during the initiation of muscle contraction. Besides its antioxidant and anti-inflammatory effects CrM also upregulates IGF-1 resulting in hyperthophy with an increase in muscle function. However, it is unknown whether CrM supplementation during resistance training would revert the negative effects of high-fat diet on the muscle performance. During 8 weeks we measured muscle performance to climb a 1.1m and 80 degrees ladder with increasing load on trained rats that had received standard diet or high-fat diet, supplemented or not with CrM. We observed that the CrM supplementation up-regulated IGF-1 and phospho-AKT protein levels, suggesting an activation of the IGF1P13K-Akt/PKB-mTOR pathway. Moreover, despite the CrM supplementation, HF diet downregulated several proteins of the IGF1-PI3K-Akt/PKB-mTOR pathway, suggesting that diet lipid content is crucial to maintain or improve muscle function during resistance training.en
dc.description.affiliationSao Paulo State Univ UNESP, Inst Biosci Botucatu, Dept Anat, Botucatu, SP, Brazil
dc.description.affiliationCtr Univ Adventista Sao Paulo, Lab Phys Act Metab & Hlth, Sao Paulo, Brazil
dc.description.affiliationFMJ, Dept Morphol & Basic Pathol, Sao Paulo, Brazil
dc.description.affiliationESEF, Sao Paulo, Brazil
dc.description.affiliationUniv Metodista Piracicaba, Lab Neuromuscular Plast, Grad Program Sci Human Movement, Sao Paulo, Brazil
dc.description.affiliationHeidelberg Univ Hosp, Inst Physiol & Pathophysiol, Cardioventilatory Muscle Physiol Lab, Heidelberg, Germany
dc.description.affiliationUnespSao Paulo State Univ UNESP, Inst Biosci Botucatu, Dept Anat, Botucatu, SP, Brazil
dc.format.extent20
dc.identifierhttp://dx.doi.org/10.1371/journal.pone.0199728
dc.identifier.citationPlos One. San Francisco: Public Library Science, v. 13, n. 10, 20 p., 2018.
dc.identifier.doi10.1371/journal.pone.0199728
dc.identifier.issn1932-6203
dc.identifier.lattes3681613160086175
dc.identifier.lattes8198771998347483
dc.identifier.orcid0000-0003-3944-1906
dc.identifier.orcid0000-0002-7237-7021
dc.identifier.urihttp://hdl.handle.net/11449/184901
dc.identifier.wosWOS:000446383500001
dc.language.isoeng
dc.publisherPublic Library Science
dc.relation.ispartofPlos One
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.titleHigh-fat diet suppresses the positive effect of creatine supplementation on skeletal muscle function by reducing protein expression of IGF-PI3K-AKT-mTOR pathwayen
dc.typeArtigo
dcterms.rightsHolderPublic Library Science
unesp.author.lattes3681613160086175[1]
unesp.author.lattes8198771998347483[6]
unesp.author.orcid0000-0003-3944-1906[1]
unesp.author.orcid0000-0002-2477-8242[2]
unesp.author.orcid0000-0001-7744-9138[8]
unesp.author.orcid0000-0002-7237-7021[6]

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