{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1363670320650020352.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1139/h07-149"}},{"identifier":{"@type":"URI","@value":"http://www.nrcresearchpress.com/doi/full-xml/10.1139/H07-149"}},{"identifier":{"@type":"URI","@value":"http://www.nrcresearchpress.com/doi/pdf/10.1139/H07-149"}}],"dc:title":[{"@value":"A chronic increase in physical activity inhibits fed-state mTOR/S6K1 signaling and reduces IRS-1 serine phosphorylation in rat skeletal muscle"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>A chronic increase in physical activity and (or) endurance training can improve insulin sensitivity in insulin-resistant skeletal muscle. Cellular mechanisms responsible for the development of insulin resistance are unclear, though one proposed mechanism is that nutrient overload chronically increases available energy, over-activating the mammalian target of rapamycin (mTOR) and ribosomal S6 kinase 1 (S6K1) signaling pathway leading to increased phosphorylation of serine residues on insulin receptor substrate-1 (IRS-1). The objective of this study was to determine if increased physical activity would inhibit mTOR/S6K1 signaling and reduce IRS-1 serine phosphorylation in rat skeletal muscle. Soleus muscle was collected from fed male Sprague–Dawley sedentary rats (Inactive) and rats with free access to running wheels for 9 weeks (Active). Immunoblotting methods were used to measure phosphorylation status of mTOR, S6K1, IRS-1, and PKB/Akt (protein kinase B/AKT), and total abundance of proteins associated with the mTOR pathway. Muscle citrate synthase activity and plasma insulin and glucose concentrations were measured. Phosphorylation of mTOR (Ser<jats:sub>2448</jats:sub>), S6K1 (Thr<jats:sub>389</jats:sub>), and IRS-1 (Ser<jats:sub>636–639</jats:sub>) was reduced in Active rats (p < 0.05). Total protein abundance of mTOR, S6K1, IRS-1, 4E-BP1, eEF2, PKB/Akt and AMPKα, and phosphorylation of PKB/Akt were unaffected (p > 0.05). Total SKAR protein, a downstream target of S6K1, and citrate synthase activity increased in Active rats (p < 0.05), though plasma insulin and glucose levels were unchanged (p > 0.05). Reduced mTOR/S6K1 signaling during chronic increases in physical activity may play an important regulatory role in the serine phosphorylation of IRS-1, which should be examined as a potential mechanism for attenuation of insulin resistance associated with increased IRS-1 serine phosphorylation.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1383670320650020353","@type":"Researcher","foaf:name":[{"@value":"Erin L. Glynn"}],"jpcoar:affiliationName":[{"@value":"Division of Rehabilitation Sciences, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."},{"@value":"Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA."},{"@value":"Department of Physical Therapy, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320650020357","@type":"Researcher","foaf:name":[{"@value":"Heidi L. Lujan"}],"jpcoar:affiliationName":[{"@value":"Division of Rehabilitation Sciences, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."},{"@value":"Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA."},{"@value":"Department of Physical Therapy, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320650020354","@type":"Researcher","foaf:name":[{"@value":"Victoria J. Kramer"}],"jpcoar:affiliationName":[{"@value":"Division of Rehabilitation Sciences, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."},{"@value":"Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA."},{"@value":"Department of Physical Therapy, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320650020356","@type":"Researcher","foaf:name":[{"@value":"Micah J. Drummond"}],"jpcoar:affiliationName":[{"@value":"Division of Rehabilitation Sciences, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."},{"@value":"Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA."},{"@value":"Department of Physical Therapy, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320650020352","@type":"Researcher","foaf:name":[{"@value":"Stephen E. DiCarlo"}],"jpcoar:affiliationName":[{"@value":"Division of Rehabilitation Sciences, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."},{"@value":"Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA."},{"@value":"Department of Physical Therapy, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320650020355","@type":"Researcher","foaf:name":[{"@value":"Blake B. Rasmussen"}],"jpcoar:affiliationName":[{"@value":"Division of Rehabilitation Sciences, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."},{"@value":"Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA."},{"@value":"Department of Physical Therapy, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1144, USA."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"17155312"},{"@type":"EISSN","@value":"17155320"}],"prism:publicationName":[{"@value":"Applied Physiology, Nutrition, and Metabolism"}],"dc:publisher":[{"@value":"Canadian Science Publishing"}],"prism:publicationDate":"2008-02","prism:volume":"33","prism:number":"1","prism:startingPage":"93","prism:endingPage":"101"},"reviewed":"false","dc:rights":["http://www.nrcresearchpress.com/page/about/CorporateTextAndDataMining"],"url":[{"@id":"http://www.nrcresearchpress.com/doi/full-xml/10.1139/H07-149"},{"@id":"http://www.nrcresearchpress.com/doi/pdf/10.1139/H07-149"}],"createdAt":"2008-03-17","modifiedAt":"2021-09-06","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360009142470261760","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Enhanced skeletal muscle insulin sensitivity after acute resistance-type exercise is upregulated by rapamycin-sensitive mTOR complex 1 inhibition"}]},{"@id":"https://cir.nii.ac.jp/crid/1390585636769671296","@type":"Article","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"発育期における長期間の自発走運動とカロリー制限が雌ラット骨格筋の細胞内シグナル伝達に及ぼす影響"},{"@language":"en","@value":"Effects of long-term voluntary running exercise and caloric restriction during development on intracellular signaling in female rat skeletal muscles"},{"@language":"ja-Kana","@value":"ハツイクキ ニ オケル チョウキカン ノ ジハツソウ ウンドウ ト カロリー セイゲン ガ メス ラット コッカクキン ノ サイボウ ナイ シグナル デンタツ ニ オヨボス エイキョウ"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1139/h07-149"},{"@type":"CROSSREF","@value":"10.1038/s41598-020-65397-z_references_DOI_H0Ck90PcfNcQhyqpHc3TGeBg8Fp"},{"@type":"CROSSREF","@value":"10.7600/jspfsm.74.155_references_DOI_H0Ck90PcfNcQhyqpHc3TGeBg8Fp"}]}