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dc.creatorStančić, Ana
dc.creatorFilipović, Miloš
dc.creatorIvanović-Burmazović, Ivana
dc.creatorMašović, Sava
dc.creatorJanković, Aleksandra
dc.creatorOtašević, Vesna
dc.creatorKorać, Aleksandra
dc.creatorBuzadžić, Biljana
dc.creatorKorać, Bato
dc.date.accessioned2017-11-23T11:28:48Z
dc.date.available2900-01-01
dc.date.issued2017
dc.identifier.issn0009-2797
dc.identifier.urihttp://linkinghub.elsevier.com/retrieve/pii/S0009279717300030
dc.identifier.urihttps://ibiss-r.rcub.bg.ac.rs/handle/123456789/2766
dc.description.abstractConsidering the vital role of skeletal muscle in control of whole-body metabolism and the severity of long-term diabetic complications, we aimed to reveal the molecular pattern of early diabetes-related skeletal muscle phenotype in terms of energy metabolism, focusing on regulatory mechanisms, and the possibility to improve it using two redox modulators, L-arginine and superoxide dismutase (SOD) mimic. Alloxan-induced diabetic rats (120 mg/kg) were treated with L-arginine or the highly specific SOD mimic, M40403, for 7 days. As appropriate controls, non-diabetic rats received the same treatments. We found that L-arginine and M40403 restored diabetes-induced impairment of phospho-5′-AMP-activated protein kinase α (AMPKα) signaling by upregulating AMPKα protein itself and its downstream effectors, peroxisome proliferator-activated receptor-γ coactivator-1α and nuclear respiratory factor 1. Also, there was a restitution of the protein levels of oxidative phosphorylation components (complex I, complex II and complex IV) and mitofusin 2. Furthermore, L-arginine and M40403 induced translocation of glucose transporter 4 to the membrane and upregulation of protein of phosphofructokinase and acyl coenzyme A dehydrogenase, diminishing negative diabetic effects on limiting factors of glucose and lipid metabolism. Both treatments abolished diabetes-induced downregulation of sarcoplasmic reticulum calcium-ATPase proteins (SERCA 1 and 2). Similar effects of L-arginine and SOD mimic treatments suggest that disturbances in the superoxide/nitric oxide ratio may be responsible for skeletal muscle mitochondrial and metabolic impairment in early diabetes. Our results provide evidence that L-arginine and SOD mimics have potential in preventing and treating metabolic disturbances accompanying this widespread metabolic disease.
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173054/RS//
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173055/RS//
dc.relationEuropean Cooperation in Science and Research (COST Action BM1203)
dc.rightsrestrictedAccess
dc.sourceChemico-Biological Interactions
dc.subjectDiabetes
dc.subjectSkeletal muscle
dc.subjectRedox regulation
dc.subjectL-Arginine
dc.subjectSOD mimic
dc.titleEarly energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic
dc.typearticle
dc.rights.licenseARR
dcterms.abstractОташевић, Весна; Кораћ, Бато; Бузаджић, Биљана; Кораћ, Aлександра; Јанковић, Aлександра; Машовић, Сава; Ивановић-Бурмазовић, Ивана; Филиповић, Милош; Станчић, Aна;
dc.rights.holder© 2017 Elsevier B.V.
dc.citation.volume272
dc.description.otherChemico-Biological Interactions (2017), 272: 188-196
dc.identifier.doi10.1016/j.cbi.2017.05.003
dc.identifier.pmid28483572
dc.identifier.scopus2-s2.0-85019714424
dc.identifier.wos000404198300021
dc.citation.apaStancic, A., Filipovic, M., Ivanovic-Burmazovic, I., Masovic, S., Jankovic, A., Otasevic, V., Korac, A., et al. (2017). Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic. Chemico-Biological Interactions, 272, 188–196.
dc.citation.vancouverStancic A, Filipovic M, Ivanovic-Burmazovic I, Masovic S, Jankovic A, Otasevic V, Korac A, Buzadzic B, Korac B. Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic. Chem Biol Interact. 2017;272:188–96.
dc.citation.spage188
dc.citation.epage196
dc.type.versionpublishedVersionen
dc.citation.rankM22


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