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 . .

TY  - JOUR
AU  - Hmaid, Amal AAA
AU  - Markelić, Milica
AU  - Otašević, Vesna
AU  - Mašović, Sava
AU  - Janković, Aleksandra
AU  - Korać, Bato
AU  - Korać, Aleksandra
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6212
AB  - Structural changes affecting cardiomyocyte function may contribute to the pathophysiological remodeling underlying cardiac function impairment. Recent reports have shown that endogenous nitric oxide (NO) plays an important role in this process. In order to examine the role of NO in cardiomyocyte remodeling, male rats were acclimated to room temperature (22 ± 1 °C) or cold (4 ± 1 °C) and treated with 2.25% l-arginine·HCl or 0.01% l-NAME (Nω-nitro-l-arginine methyl ester)·HCl for 45 days. Untreated groups served as controls. Right heart ventricles were routinely prepared for light microscopic examination. Stereological estimations of volume densities of cardiomyocytes, surrounding blood vessels and connective tissue, as well as the morphometric measurements of cardiomyocyte diameters were performed. Tissue sections were also analyzed for structural alterations. We observed that both l-arginine and l-NAME supplementation induced cardiomyocyte hypertrophy, regardless of ambient temperature. However, cardiomyocyte hypertrophy was associated with fibrosis and extra collagen deposition only in the l-NAME treated group. Taken together, our results suggest that NO has a modulatory role in right heart ventricle remodeling by coordinating hypertrophy of cardiomyocytes and fibrous tissue preventing cardiac fibrosis.
PB  - Elsevier
T2  - Saudi Journal of Biological Sciences
T1  - Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation
IS  - 3
VL  - 25
DO  - 10.1016/j.sjbs.2016.01.022
SP  - 537
EP  - 544
ER  - 

@article{
author = "Hmaid, Amal AAA and Markelić, Milica and Otašević, Vesna and Mašović, Sava and Janković, Aleksandra and Korać, Bato and Korać, Aleksandra",
year = "2016",
abstract = "Structural changes affecting cardiomyocyte function may contribute to the pathophysiological remodeling underlying cardiac function impairment. Recent reports have shown that endogenous nitric oxide (NO) plays an important role in this process. In order to examine the role of NO in cardiomyocyte remodeling, male rats were acclimated to room temperature (22 ± 1 °C) or cold (4 ± 1 °C) and treated with 2.25% l-arginine·HCl or 0.01% l-NAME (Nω-nitro-l-arginine methyl ester)·HCl for 45 days. Untreated groups served as controls. Right heart ventricles were routinely prepared for light microscopic examination. Stereological estimations of volume densities of cardiomyocytes, surrounding blood vessels and connective tissue, as well as the morphometric measurements of cardiomyocyte diameters were performed. Tissue sections were also analyzed for structural alterations. We observed that both l-arginine and l-NAME supplementation induced cardiomyocyte hypertrophy, regardless of ambient temperature. However, cardiomyocyte hypertrophy was associated with fibrosis and extra collagen deposition only in the l-NAME treated group. Taken together, our results suggest that NO has a modulatory role in right heart ventricle remodeling by coordinating hypertrophy of cardiomyocytes and fibrous tissue preventing cardiac fibrosis.",
publisher = "Elsevier",
journal = "Saudi Journal of Biological Sciences",
title = "Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation",
number = "3",
volume = "25",
doi = "10.1016/j.sjbs.2016.01.022",
pages = "537-544"
}

Hmaid, A. A., Markelić, M., Otašević, V., Mašović, S., Janković, A., Korać, B.,& Korać, A.. (2016). Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation. in Saudi Journal of Biological Sciences
Elsevier., 25(3), 537-544.
https://doi.org/10.1016/j.sjbs.2016.01.022

Hmaid AA, Markelić M, Otašević V, Mašović S, Janković A, Korać B, Korać A. Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation. in Saudi Journal of Biological Sciences. 2016;25(3):537-544.
doi:10.1016/j.sjbs.2016.01.022 .

Hmaid, Amal AAA, Markelić, Milica, Otašević, Vesna, Mašović, Sava, Janković, Aleksandra, Korać, Bato, Korać, Aleksandra, "Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation" in Saudi Journal of Biological Sciences, 25, no. 3 (2016):537-544,
https://doi.org/10.1016/j.sjbs.2016.01.022 . .