TY  - JOUR
AU  - Stančić, Ana
AU  - Filipović, Miloš
AU  - Ivanović-Burmazović, Ivana
AU  - Mašović, Sava
AU  - Janković, Aleksandra
AU  - Otašević, Vesna
AU  - Korać, Aleksandra
AU  - Buzadžić, Biljana
AU  - Korać, Bato
PY  - 2017
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0009279717300030
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2766
AB  - Considering 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.
T2  - Chemico-Biological Interactions
T1  - Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic
VL  - 272
DO  - 10.1016/j.cbi.2017.05.003
SP  - 188
EP  - 196
ER  - 

@article{
author = "Stančić, Ana and Filipović, Miloš and Ivanović-Burmazović, Ivana and Mašović, Sava and Janković, Aleksandra and Otašević, Vesna and Korać, Aleksandra and Buzadžić, Biljana and Korać, Bato",
year = "2017",
abstract = "Considering 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.",
journal = "Chemico-Biological Interactions",
title = "Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic",
volume = "272",
doi = "10.1016/j.cbi.2017.05.003",
pages = "188-196"
}

Stančić, A., Filipović, M., Ivanović-Burmazović, I., Mašović, S., Janković, A., Otašević, V., Korać, A., Buzadžić, B.,& Korać, B.. (2017). Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic. in Chemico-Biological Interactions, 272, 188-196.
https://doi.org/10.1016/j.cbi.2017.05.003

Stančić A, Filipović M, Ivanović-Burmazović I, Mašović S, Janković A, Otašević V, Korać A, Buzadžić B, Korać B. Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic. in Chemico-Biological Interactions. 2017;272:188-196.
doi:10.1016/j.cbi.2017.05.003 .

Stančić, Ana, Filipović, Miloš, Ivanović-Burmazović, Ivana, Mašović, Sava, Janković, Aleksandra, Otašević, Vesna, Korać, Aleksandra, Buzadžić, Biljana, Korać, Bato, "Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic" in Chemico-Biological Interactions, 272 (2017):188-196,
https://doi.org/10.1016/j.cbi.2017.05.003 . .