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dc.contributor.authorNissinen, Tuuli
dc.date.accessioned2014-10-02T11:55:13Z
dc.date.available2014-10-02T11:55:13Z
dc.date.issued2014
dc.identifier.otheroai:jykdok.linneanet.fi:1446402
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/44371
dc.description.abstractInsulin is a hormone that plays an important role in the regulation of the metabolism of all the main nutrients. Its main function is to stimulate glucose uptake and disposal or utilization by the cells and thus to decrease blood glucose concentration. However, it also inhibits breakdown of proteins and lipids and promotes their synthesis. Type 1 diabetes is a disease in which insulin secretion is impaired because of destruction of pancreatic β-cells. It is characterized by hyperglycemia and increased reliance on fat oxidation. This is seen also as altered gene expression patterns. The purpose of this study was to look into the effects of insulin deficiency on exercise-induced acute responses in the expression of genes and the activation of signaling pathways involved in fatty acid oxidation. Male NMRI mice (n = 64) were randomly assigned into three streptozotocin-induced diabetic and three healthy groups. Two healthy and two diabetic groups performed a single one-hour bout of treadmill running (21 m/min, 2.5o incline) and were sacrificed either three or six hours after exercise. Gastrocnemius muscles were dissected and mRNA expression and protein expression and phosphorylation were analyzed with RT-PCR and Western blotting respectively. PGC-1α mRNA expression increased (p < 0.001) after exercise in both healthy and diabetic mice, but the response was higher in diabetic mice (p < 0.05). PDK4 mRNA expression increased after exercise only in diabetic mice (p < 0.05). Diabetic mice showed a more pronounced response in CPT1B mRNA six hours after exercise compared with healthy exercised mice (p < 0.05). Contrary to mRNA level results, PGC-1α protein content did not change in response to exercise when compared with sedentary counterparts of the same health status. The analysis of AMPK and p38 MAPK phosphorylation did not suggest activation of these pathways in response to exercise. Even a decrease in AMPK phosphorylation was seen six hours after exercise in healthy mice (p < 0.05) while p38 MAPK phosphorylation was de-creased in diabetic mice three hours after exercise (p < 0.05). There were no significant changes in proteins PDK4, CPT1B, sirtuins 1, 3 and 6, ACC or Cyt c. These results suggest that diabetic mice have more pronounced exercise-induced responses in the expression of genes related to increased fatty acid oxidation. These changes may be mediated by in-creased PGC-1α activation as no increases were seen in PGC-1α protein expression. The time points were not optimal for protein level analyses and thus, further studies are needed to clarify protein phosphorylation and expression changes and to find out whether the gene expression changes are reflected to the level of substrate metabolism.en
dc.format.extent1 verkkoaineisto (102 sivua)
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.rightsThis publication is copyrighted. You may download, display and print it for Your own personal use. Commercial use is prohibited.en
dc.rightsJulkaisu on tekijänoikeussäännösten alainen. Teosta voi lukea ja tulostaa henkilökohtaista käyttöä varten. Käyttö kaupallisiin tarkoituksiin on kielletty.fi
dc.subject.otherexercise
dc.subject.otherdiabetes
dc.subject.otherinsulin
dc.subject.otherfatty acid oxidation
dc.titleEffects of insulin deficiency on exercise-induced acute responses in the regulation of fatty acid oxidation in mouse gastrocnemius muscles
dc.identifier.urnURN:NBN:fi:jyu-201410022921
dc.type.ontasotPro gradu -tutkielmafi
dc.type.ontasotMaster’s thesisen
dc.contributor.tiedekuntaLiikuntatieteellinen tiedekuntafi
dc.contributor.tiedekuntaFaculty of Sport and Health Sciencesen
dc.contributor.laitosLiikuntabiologian laitosfi
dc.contributor.laitosDepartment of Biology of Physical Activityen
dc.contributor.yliopistoUniversity of Jyväskyläen
dc.contributor.yliopistoJyväskylän yliopistofi
dc.contributor.oppiaineLiikuntafysiologiafi
dc.contributor.oppiaineExercise Physiologyen
dc.date.updated2014-10-02T11:55:14Z
dc.rights.accesslevelopenAccessfi
dc.type.publicationmasterThesis
dc.contributor.oppiainekoodi5011
dc.subject.ysoliikunta
dc.subject.ysodiabetes
dc.subject.ysoinsuliini
dc.subject.ysorasvahapot
dc.subject.ysohapettuminen
dc.format.contentfulltext
dc.type.okmG2


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