Tepavčević, Snežana

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Authority KeyName Variants
orcid::0000-0002-5758-070X
  • Tepavčević, Snežana (32)
  • Radivojša, Snežana (2)
Projects

Author's Bibliography

Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium–potassium pump in the hearts of male rats

Romić, Snježana Đ.; Đorđević, Ana; Tepavčević, Snežana; Ćulafić, Tijana; Stojiljković, Mojca D.; Bursać, Biljana; Stanišić, Jelena; Kostić, Milan; Gligorovska, Ljupka; Korićanac, Goran

(2020)

TY  - JOUR
AU  - Romić, Snježana Đ.
AU  - Đorđević, Ana
AU  - Tepavčević, Snežana
AU  - Ćulafić, Tijana
AU  - Stojiljković, Mojca D.
AU  - Bursać, Biljana
AU  - Stanišić, Jelena
AU  - Kostić, Milan
AU  - Gligorovska, Ljupka
AU  - Korićanac, Goran
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8849
AB  - Both a diet rich in fructose and chronic stress exposure induce metabolic and cardiovascular disturbances. The aim of this study was to examine the effects of the fructose-rich diet and chronic stress, separately and in combination, on insulin signaling and molecules regulating glycogen synthesis and ion transport in the heart, and to reveal whether these effects coincide with changes in glucocorticoid receptor (GR) activation. Male Wistar rats were subjected to 10% fructose in drinking water and/or to chronic unpredictable stress for 9 weeks. Protein expression and/or phosphorylation of the insulin receptor (IR), protein tyrosine phosphatase 1B, insulin receptor substrate 1 (IRS1), protein kinase B (Akt), extracellular signal-regulated kinase 1/2 (ERK1/2), glycogen synthase kinase-3β (GSK-3β) and Na+/K+-ATPase α-subunits in cardiac tissue were analyzed by western blot. GR distribution between cytosolic and nuclear fractions was also analyzed. The fructose-rich diet decreased the level of pERK1/2 (Thr202/Tyr204) and pGSK-3β (Ser9) independently of stress, while chronic stress increased the IRS1 content and prevented the fructose diet-induced decrease of the pAkt (Ser473) level. The fructose-rich diet in combination with chronic stress reduced the protein content of cardiac IR and attenuated IRS1 upregulation. Separate treatments increased the protein content of Na+/K+-ATPase α1- and α2-subunits, while after combined treatment the α2 content was at the control level and the α1 content was lower than the control level. The effect of combined treatment on cardiac IR and α2-subunit expression could be mediated by increased GR nuclear accumulation. Our study provides new insights into the effects of chronic stress and a combination of the fructose diet and chronic stress on the studied molecules in the heart.
T2  - Food & Function
T1  - Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium–potassium pump in the hearts of male rats
VL  - 11
IS  - 2
SP  - 1455
EP  - 1466
DO  - 10.1039/C9FO02306B
ER  - 
@article{
author = "Romić, Snježana Đ. and Đorđević, Ana and Tepavčević, Snežana and Ćulafić, Tijana and Stojiljković, Mojca D. and Bursać, Biljana and Stanišić, Jelena and Kostić, Milan and Gligorovska, Ljupka and Korićanac, Goran",
year = "2020",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/8849",
abstract = "Both a diet rich in fructose and chronic stress exposure induce metabolic and cardiovascular disturbances. The aim of this study was to examine the effects of the fructose-rich diet and chronic stress, separately and in combination, on insulin signaling and molecules regulating glycogen synthesis and ion transport in the heart, and to reveal whether these effects coincide with changes in glucocorticoid receptor (GR) activation. Male Wistar rats were subjected to 10% fructose in drinking water and/or to chronic unpredictable stress for 9 weeks. Protein expression and/or phosphorylation of the insulin receptor (IR), protein tyrosine phosphatase 1B, insulin receptor substrate 1 (IRS1), protein kinase B (Akt), extracellular signal-regulated kinase 1/2 (ERK1/2), glycogen synthase kinase-3β (GSK-3β) and Na+/K+-ATPase α-subunits in cardiac tissue were analyzed by western blot. GR distribution between cytosolic and nuclear fractions was also analyzed. The fructose-rich diet decreased the level of pERK1/2 (Thr202/Tyr204) and pGSK-3β (Ser9) independently of stress, while chronic stress increased the IRS1 content and prevented the fructose diet-induced decrease of the pAkt (Ser473) level. The fructose-rich diet in combination with chronic stress reduced the protein content of cardiac IR and attenuated IRS1 upregulation. Separate treatments increased the protein content of Na+/K+-ATPase α1- and α2-subunits, while after combined treatment the α2 content was at the control level and the α1 content was lower than the control level. The effect of combined treatment on cardiac IR and α2-subunit expression could be mediated by increased GR nuclear accumulation. Our study provides new insights into the effects of chronic stress and a combination of the fructose diet and chronic stress on the studied molecules in the heart.",
journal = "Food & Function",
title = "Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium–potassium pump in the hearts of male rats",
volume = "11",
number = "2",
pages = "1455-1466",
doi = "10.1039/C9FO02306B"
}
Romić, S. Đ., Đorđević, A., Tepavčević, S., Ćulafić, T., Stojiljković, M. D., Bursać, B., Stanišić, J., Kostić, M., Gligorovska, L.,& Korićanac, G. (2020). Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium–potassium pump in the hearts of male rats.
Food & Function, 11(2), 1455-1466.
https://doi.org/10.1039/C9FO02306B
Romić SĐ, Đorđević A, Tepavčević S, Ćulafić T, Stojiljković MD, Bursać B, Stanišić J, Kostić M, Gligorovska L, Korićanac G. Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium–potassium pump in the hearts of male rats. Food & Function. 2020;11(2):1455-1466
Romić Snježana Đ., Đorđević Ana, Tepavčević Snežana, Ćulafić Tijana, Stojiljković Mojca D., Bursać Biljana, Stanišić Jelena, Kostić Milan, Gligorovska Ljupka, Korićanac Goran, "Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium–potassium pump in the hearts of male rats" Food & Function, 11, no. 2 (2020):1455-1466,
https://doi.org/10.1039/C9FO02306B .
1
1
1

The role of the adenosine triphosphate-sensitive potassium channels in pinacidil-induced vasodilatation of the human saphenous vein in patients with and without type 2 diabetes mellitus

Rajković, Jovana; Perić, M.; Stanišić, Jelena; Novaković, Radmila; Đokić, Vladimir; Rakočević, Jelena; Tepavčević, Snežana; Labudović-Borović, Milica; Gostimirović, Miloš; Heinle, Helmut; Gojković-Bukarica, Ljiljana

(2020)

TY  - JOUR
AU  - Rajković, Jovana
AU  - Perić, M.
AU  - Stanišić, Jelena
AU  - Novaković, Radmila
AU  - Đokić, Vladimir
AU  - Rakočević, Jelena
AU  - Tepavčević, Snežana
AU  - Labudović-Borović, Milica
AU  - Gostimirović, Miloš
AU  - Heinle, Helmut
AU  - Gojković-Bukarica, Ljiljana
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9054
AB  - Type 2 diabetes mellitus (T2DM) increases cardiovascular complications. Diabetic vascular dysfunction is associated with the reduced activity of the different smooth muscle potassium (K+) channels. Thus, the objective of our study was to investigate the role of the adenosine triphosphate (ATP)-sensitive K+ (KATP) channels in the relaxant effect of potassium channel opener, pinacidil on the human saphenous vein (HSV) obtained from the patients with and without T2DM. The rings of HSV without the endothelium, obtained from the patients who had undergone coronary bypass surgery, were mounted in an organ bath system and isometric tension was recorded. The relaxation of HSV, precontracted with phenylephrine, was produced by pinacidil. The expression of KATP subunits (Kir6.1, Kir6.2 and SUR2B) was detected by immunohistochemistry and Western blot. Pinacidil produces comparable effects on HSV in patients with and without T2DM. The suppression of pinacidil effect and its maximal relaxation by glibenclamide, selective blocker of KATP channels, was more pronounced on HSV in patients without T2DM. All three types of KATP subunits are expressed on the smooth muscle cells of HSV. While there are no differences in the expression of Kir6.1 and Kir6.2, the expression of SUR2B is lower in HSV in patients with T2DM. Pinacidil produced comparable KATP-dependent and -independent relaxation of the HSV in patients with/without T2DM. According to the effect of glibenclamide and the applied molecular analysis, presented findings demonstrated that diabetes mellitus was associated with the reduced expression of SUR2B subunit in the vascular smooth muscle of HSV.
T2  - Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
T1  - The role of the adenosine triphosphate-sensitive potassium channels in pinacidil-induced vasodilatation of the human saphenous vein in patients with and without type 2 diabetes mellitus
VL  - 71
IS  - 1
DO  - 10.26402/jpp.2020.1.12
ER  - 
@article{
author = "Rajković, Jovana and Perić, M. and Stanišić, Jelena and Novaković, Radmila and Đokić, Vladimir and Rakočević, Jelena and Tepavčević, Snežana and Labudović-Borović, Milica and Gostimirović, Miloš and Heinle, Helmut and Gojković-Bukarica, Ljiljana",
year = "2020",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/9054",
abstract = "Type 2 diabetes mellitus (T2DM) increases cardiovascular complications. Diabetic vascular dysfunction is associated with the reduced activity of the different smooth muscle potassium (K+) channels. Thus, the objective of our study was to investigate the role of the adenosine triphosphate (ATP)-sensitive K+ (KATP) channels in the relaxant effect of potassium channel opener, pinacidil on the human saphenous vein (HSV) obtained from the patients with and without T2DM. The rings of HSV without the endothelium, obtained from the patients who had undergone coronary bypass surgery, were mounted in an organ bath system and isometric tension was recorded. The relaxation of HSV, precontracted with phenylephrine, was produced by pinacidil. The expression of KATP subunits (Kir6.1, Kir6.2 and SUR2B) was detected by immunohistochemistry and Western blot. Pinacidil produces comparable effects on HSV in patients with and without T2DM. The suppression of pinacidil effect and its maximal relaxation by glibenclamide, selective blocker of KATP channels, was more pronounced on HSV in patients without T2DM. All three types of KATP subunits are expressed on the smooth muscle cells of HSV. While there are no differences in the expression of Kir6.1 and Kir6.2, the expression of SUR2B is lower in HSV in patients with T2DM. Pinacidil produced comparable KATP-dependent and -independent relaxation of the HSV in patients with/without T2DM. According to the effect of glibenclamide and the applied molecular analysis, presented findings demonstrated that diabetes mellitus was associated with the reduced expression of SUR2B subunit in the vascular smooth muscle of HSV.",
journal = "Journal of physiology and pharmacology : an official journal of the Polish Physiological Society",
title = "The role of the adenosine triphosphate-sensitive potassium channels in pinacidil-induced vasodilatation of the human saphenous vein in patients with and without type 2 diabetes mellitus",
volume = "71",
number = "1",
doi = "10.26402/jpp.2020.1.12"
}
Rajković, J., Perić, M., Stanišić, J., Novaković, R., Đokić, V., Rakočević, J., Tepavčević, S., Labudović-Borović, M., Gostimirović, M., Heinle, H.,& Gojković-Bukarica, L. (2020). The role of the adenosine triphosphate-sensitive potassium channels in pinacidil-induced vasodilatation of the human saphenous vein in patients with and without type 2 diabetes mellitus.
Journal of physiology and pharmacology : an official journal of the Polish Physiological Society, 71(1).
https://doi.org/10.26402/jpp.2020.1.12
Rajković J, Perić M, Stanišić J, Novaković R, Đokić V, Rakočević J, Tepavčević S, Labudović-Borović M, Gostimirović M, Heinle H, Gojković-Bukarica L. The role of the adenosine triphosphate-sensitive potassium channels in pinacidil-induced vasodilatation of the human saphenous vein in patients with and without type 2 diabetes mellitus. Journal of physiology and pharmacology : an official journal of the Polish Physiological Society. 2020;71(1)
Rajković Jovana, Perić M., Stanišić Jelena, Novaković Radmila, Đokić Vladimir, Rakočević Jelena, Tepavčević Snežana, Labudović-Borović Milica, Gostimirović Miloš, Heinle Helmut, Gojković-Bukarica Ljiljana, "The role of the adenosine triphosphate-sensitive potassium channels in pinacidil-induced vasodilatation of the human saphenous vein in patients with and without type 2 diabetes mellitus" Journal of physiology and pharmacology : an official journal of the Polish Physiological Society, 71, no. 1 (2020),
https://doi.org/10.26402/jpp.2020.1.12 .
1

Involvement of large-conductance calcium-activated potassium channels in pinacidil effects on the isolated bypass grafts from patients with and without type-2 diabetes mellitus

Rajković, Jovana; Perić, Miodrag; Stanišić, Jelena; Rakočević, Jelena T.; Novaković, Radmila; Đokić, Vladimir; Labudović-Borović, Milica; Tepavčević, Snežana; Heinle, Helmut; Gojković-Bukarica, Ljiljana

(2018)

TY  - CONF
AU  - Rajković, Jovana
AU  - Perić, Miodrag
AU  - Stanišić, Jelena
AU  - Rakočević, Jelena T.
AU  - Novaković, Radmila
AU  - Đokić, Vladimir
AU  - Labudović-Borović, Milica
AU  - Tepavčević, Snežana
AU  - Heinle, Helmut
AU  - Gojković-Bukarica, Ljiljana
PY  - 2018
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7912
C3  - European Journal of Clinical Investigation
T1  - Involvement of large-conductance calcium-activated potassium channels in pinacidil effects on the isolated bypass grafts from patients with and without type-2 diabetes mellitus
VL  - 48
IS  - SI (Suppl. 1)
SP  - 137
ER  - 
@conference{
author = "Rajković, Jovana and Perić, Miodrag and Stanišić, Jelena and Rakočević, Jelena T. and Novaković, Radmila and Đokić, Vladimir and Labudović-Borović, Milica and Tepavčević, Snežana and Heinle, Helmut and Gojković-Bukarica, Ljiljana",
year = "2018",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/7912",
journal = "European Journal of Clinical Investigation",
title = "Involvement of large-conductance calcium-activated potassium channels in pinacidil effects on the isolated bypass grafts from patients with and without type-2 diabetes mellitus",
volume = "48",
number = "SI (Suppl. 1)",
pages = "137"
}
Rajković, J., Perić, M., Stanišić, J., Rakočević, J. T., Novaković, R., Đokić, V., Labudović-Borović, M., Tepavčević, S., Heinle, H.,& Gojković-Bukarica, L. (2018). Involvement of large-conductance calcium-activated potassium channels in pinacidil effects on the isolated bypass grafts from patients with and without type-2 diabetes mellitus.
European Journal of Clinical Investigation, 48(SI (Suppl. 1)), 137.
Rajković J, Perić M, Stanišić J, Rakočević JT, Novaković R, Đokić V, Labudović-Borović M, Tepavčević S, Heinle H, Gojković-Bukarica L. Involvement of large-conductance calcium-activated potassium channels in pinacidil effects on the isolated bypass grafts from patients with and without type-2 diabetes mellitus. European Journal of Clinical Investigation. 2018;48(SI (Suppl. 1)):137
Rajković Jovana, Perić Miodrag, Stanišić Jelena, Rakočević Jelena T., Novaković Radmila, Đokić Vladimir, Labudović-Borović Milica, Tepavčević Snežana, Heinle Helmut, Gojković-Bukarica Ljiljana, "Involvement of large-conductance calcium-activated potassium channels in pinacidil effects on the isolated bypass grafts from patients with and without type-2 diabetes mellitus" European Journal of Clinical Investigation, 48, no. SI (Suppl. 1) (2018):137

Involvement of atp-sensitive and large-condutance calcium-activated potassium channels in pinacidil effects on the isolated internal mammary artery grafts from patients with type-2 diabetes mellitus

Rajković, Jovana; Perić, Miodrag; Stanišić, Jelena; Rakočević, Jelena T.; Novaković, Radmila; Đokić, Vladimir; Labudović-Borović, Milica; Tepavčević, Snežana; Kanjuh, Vladimir; Heinle, Helmut; Gojković-Bukarica, Ljiljana

(2018)

TY  - CONF
AU  - Rajković, Jovana
AU  - Perić, Miodrag
AU  - Stanišić, Jelena
AU  - Rakočević, Jelena T.
AU  - Novaković, Radmila
AU  - Đokić, Vladimir
AU  - Labudović-Borović, Milica
AU  - Tepavčević, Snežana
AU  - Kanjuh, Vladimir
AU  - Heinle, Helmut
AU  - Gojković-Bukarica, Ljiljana
PY  - 2018
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0021915018307019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7949
C3  - Atherosclerosis
T1  - Involvement of atp-sensitive and large-condutance calcium-activated potassium channels in pinacidil effects on the isolated internal mammary artery grafts from patients with type-2 diabetes mellitus
VL  - 275
SP  - e133
DO  - 10.1016/j.atherosclerosis.2018.06.389
ER  - 
@conference{
author = "Rajković, Jovana and Perić, Miodrag and Stanišić, Jelena and Rakočević, Jelena T. and Novaković, Radmila and Đokić, Vladimir and Labudović-Borović, Milica and Tepavčević, Snežana and Kanjuh, Vladimir and Heinle, Helmut and Gojković-Bukarica, Ljiljana",
year = "2018",
url = "https://linkinghub.elsevier.com/retrieve/pii/S0021915018307019, http://vinar.vin.bg.ac.rs/handle/123456789/7949",
journal = "Atherosclerosis",
title = "Involvement of atp-sensitive and large-condutance calcium-activated potassium channels in pinacidil effects on the isolated internal mammary artery grafts from patients with type-2 diabetes mellitus",
volume = "275",
pages = "e133",
doi = "10.1016/j.atherosclerosis.2018.06.389"
}
Rajković, J., Perić, M., Stanišić, J., Rakočević, J. T., Novaković, R., Đokić, V., Labudović-Borović, M., Tepavčević, S., Kanjuh, V., Heinle, H.,& Gojković-Bukarica, L. (2018). Involvement of atp-sensitive and large-condutance calcium-activated potassium channels in pinacidil effects on the isolated internal mammary artery grafts from patients with type-2 diabetes mellitus.
Atherosclerosis, 275, e133.
https://doi.org/10.1016/j.atherosclerosis.2018.06.389
Rajković J, Perić M, Stanišić J, Rakočević JT, Novaković R, Đokić V, Labudović-Borović M, Tepavčević S, Kanjuh V, Heinle H, Gojković-Bukarica L. Involvement of atp-sensitive and large-condutance calcium-activated potassium channels in pinacidil effects on the isolated internal mammary artery grafts from patients with type-2 diabetes mellitus. Atherosclerosis. 2018;275:e133
Rajković Jovana, Perić Miodrag, Stanišić Jelena, Rakočević Jelena T., Novaković Radmila, Đokić Vladimir, Labudović-Borović Milica, Tepavčević Snežana, Kanjuh Vladimir, Heinle Helmut, Gojković-Bukarica Ljiljana, "Involvement of atp-sensitive and large-condutance calcium-activated potassium channels in pinacidil effects on the isolated internal mammary artery grafts from patients with type-2 diabetes mellitus" Atherosclerosis, 275 (2018):e133,
https://doi.org/10.1016/j.atherosclerosis.2018.06.389 .

Low intensity exercise prevents disturbances in insulin regulation of alpha subunits of Na plus /K plus -ATPase in the heart of fructose-fed female rats

Stanišić, Jelena; Korićanac, Goran; Stojiljković, Mirjana; Ćulafić, Tijana; Kostić, Mirjana M.; Romić, Snježana Đ.; Pantelić, Marija; Tepavčević, Snežana

(2018)

TY  - CONF
AU  - Stanišić, Jelena
AU  - Korićanac, Goran
AU  - Stojiljković, Mirjana
AU  - Ćulafić, Tijana
AU  - Kostić, Mirjana M.
AU  - Romić, Snježana Đ.
AU  - Pantelić, Marija
AU  - Tepavčević, Snežana
PY  - 2018
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7920
C3  - FEBS OPEN BIO
T1  - Low intensity exercise prevents disturbances in insulin regulation of alpha subunits of Na plus /K plus -ATPase in the heart of fructose-fed female rats
VL  - 8
IS  - Supplement 1
SP  - 224
DO  - 10.1002/2211-5463.12453
ER  - 
@conference{
author = "Stanišić, Jelena and Korićanac, Goran and Stojiljković, Mirjana and Ćulafić, Tijana and Kostić, Mirjana M. and Romić, Snježana Đ. and Pantelić, Marija and Tepavčević, Snežana",
year = "2018",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/7920",
journal = "FEBS OPEN BIO",
title = "Low intensity exercise prevents disturbances in insulin regulation of alpha subunits of Na plus /K plus -ATPase in the heart of fructose-fed female rats",
volume = "8",
number = "Supplement 1",
pages = "224",
doi = "10.1002/2211-5463.12453"
}
Stanišić, J., Korićanac, G., Stojiljković, M., Ćulafić, T., Kostić, M. M., Romić, S. Đ., Pantelić, M.,& Tepavčević, S. (2018). Low intensity exercise prevents disturbances in insulin regulation of alpha subunits of Na plus /K plus -ATPase in the heart of fructose-fed female rats.
FEBS OPEN BIO, 8(Supplement 1), 224.
https://doi.org/10.1002/2211-5463.12453
Stanišić J, Korićanac G, Stojiljković M, Ćulafić T, Kostić MM, Romić SĐ, Pantelić M, Tepavčević S. Low intensity exercise prevents disturbances in insulin regulation of alpha subunits of Na plus /K plus -ATPase in the heart of fructose-fed female rats. FEBS OPEN BIO. 2018;8(Supplement 1):224
Stanišić Jelena, Korićanac Goran, Stojiljković Mirjana, Ćulafić Tijana, Kostić Mirjana M., Romić Snježana Đ., Pantelić Marija, Tepavčević Snežana, "Low intensity exercise prevents disturbances in insulin regulation of alpha subunits of Na plus /K plus -ATPase in the heart of fructose-fed female rats" FEBS OPEN BIO, 8, no. Supplement 1 (2018):224,
https://doi.org/10.1002/2211-5463.12453 .
18
10

Moderate physical activity alters cardiac lipid metabolism of male rats on high fructose diet

Kostić, Mirjana M.; Korićanac, Goran; Tepavčević, Snežana; Ćulafić, Tijana; Romić, Snježana Đ.; Stanišić, Jelena; Pantelić, Marija; Stojiljković, Mirjana

(2018)

TY  - CONF
AU  - Kostić, Mirjana M.
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Ćulafić, Tijana
AU  - Romić, Snježana Đ.
AU  - Stanišić, Jelena
AU  - Pantelić, Marija
AU  - Stojiljković, Mirjana
PY  - 2018
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7922
C3  - FEBS OPEN BIO
T1  - Moderate physical activity alters cardiac lipid metabolism of male rats on high fructose diet
VL  - 8
IS  - Supplement 1
SP  - 223
DO  - 10.1002/2211-5463.12453
ER  - 
@conference{
author = "Kostić, Mirjana M. and Korićanac, Goran and Tepavčević, Snežana and Ćulafić, Tijana and Romić, Snježana Đ. and Stanišić, Jelena and Pantelić, Marija and Stojiljković, Mirjana",
year = "2018",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/7922",
journal = "FEBS OPEN BIO",
title = "Moderate physical activity alters cardiac lipid metabolism of male rats on high fructose diet",
volume = "8",
number = "Supplement 1",
pages = "223",
doi = "10.1002/2211-5463.12453"
}
Kostić, M. M., Korićanac, G., Tepavčević, S., Ćulafić, T., Romić, S. Đ., Stanišić, J., Pantelić, M.,& Stojiljković, M. (2018). Moderate physical activity alters cardiac lipid metabolism of male rats on high fructose diet.
FEBS OPEN BIO, 8(Supplement 1), 223.
https://doi.org/10.1002/2211-5463.12453
Kostić MM, Korićanac G, Tepavčević S, Ćulafić T, Romić SĐ, Stanišić J, Pantelić M, Stojiljković M. Moderate physical activity alters cardiac lipid metabolism of male rats on high fructose diet. FEBS OPEN BIO. 2018;8(Supplement 1):223
Kostić Mirjana M., Korićanac Goran, Tepavčević Snežana, Ćulafić Tijana, Romić Snježana Đ., Stanišić Jelena, Pantelić Marija, Stojiljković Mirjana, "Moderate physical activity alters cardiac lipid metabolism of male rats on high fructose diet" FEBS OPEN BIO, 8, no. Supplement 1 (2018):223,
https://doi.org/10.1002/2211-5463.12453 .
18
10

Disturbances in cardiac insulin signaling and nitric oxide synthase in ovariectomized rats on fructose diet can be prevented by low intensity exercise

Stanišić, Jelena; Korićanac, Goran; Stojiljković, Mojca D.; Ćulafić, Tijana; Romić, Snježana Đ.; Kostić, Mirjana M.; Pantelić, M.; Tepavčević, Snežana

(2018)

TY  - CONF
AU  - Stanišić, Jelena
AU  - Korićanac, Goran
AU  - Stojiljković, Mojca D.
AU  - Ćulafić, Tijana
AU  - Romić, Snježana Đ.
AU  - Kostić, Mirjana M.
AU  - Pantelić, M.
AU  - Tepavčević, Snežana
PY  - 2018
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0021915018309195
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7945
C3  - Atherosclerosis
T1  - Disturbances in cardiac insulin signaling and nitric oxide synthase in ovariectomized rats on fructose diet can be prevented by low intensity exercise
VL  - 275
SP  - e197
DO  - 10.1016/j.atherosclerosis.2018.06.607
ER  - 
@conference{
author = "Stanišić, Jelena and Korićanac, Goran and Stojiljković, Mojca D. and Ćulafić, Tijana and Romić, Snježana Đ. and Kostić, Mirjana M. and Pantelić, M. and Tepavčević, Snežana",
year = "2018",
url = "https://linkinghub.elsevier.com/retrieve/pii/S0021915018309195, http://vinar.vin.bg.ac.rs/handle/123456789/7945",
journal = "Atherosclerosis",
title = "Disturbances in cardiac insulin signaling and nitric oxide synthase in ovariectomized rats on fructose diet can be prevented by low intensity exercise",
volume = "275",
pages = "e197",
doi = "10.1016/j.atherosclerosis.2018.06.607"
}
Stanišić, J., Korićanac, G., Stojiljković, M. D., Ćulafić, T., Romić, S. Đ., Kostić, M. M., Pantelić, M.,& Tepavčević, S. (2018). Disturbances in cardiac insulin signaling and nitric oxide synthase in ovariectomized rats on fructose diet can be prevented by low intensity exercise.
Atherosclerosis, 275, e197.
https://doi.org/10.1016/j.atherosclerosis.2018.06.607
Stanišić J, Korićanac G, Stojiljković MD, Ćulafić T, Romić SĐ, Kostić MM, Pantelić M, Tepavčević S. Disturbances in cardiac insulin signaling and nitric oxide synthase in ovariectomized rats on fructose diet can be prevented by low intensity exercise. Atherosclerosis. 2018;275:e197
Stanišić Jelena, Korićanac Goran, Stojiljković Mojca D., Ćulafić Tijana, Romić Snježana Đ., Kostić Mirjana M., Pantelić M., Tepavčević Snežana, "Disturbances in cardiac insulin signaling and nitric oxide synthase in ovariectomized rats on fructose diet can be prevented by low intensity exercise" Atherosclerosis, 275 (2018):e197,
https://doi.org/10.1016/j.atherosclerosis.2018.06.607 .

Involvement of Atp-Sensitive Potassium Channels in Effect of Pinacidil on Saphenous Vein Obtained from the Patients with and Without Type 2 Diabetes Mellitus

Rajković, Jovana; Perić, Miodrag; Stanišić, Jelena; Rakočević, Jelena T.; Novaković, Radmila; Đokić, Vladimir; Labudović-Borović, Milica; Tepavčević, Snežana; Zivanovic, Vladimir; Kanjuh, Vladimir; Heinle, Helmut; Gojković-Bukarica, Ljiljana

(2017)

TY  - CONF
AU  - Rajković, Jovana
AU  - Perić, Miodrag
AU  - Stanišić, Jelena
AU  - Rakočević, Jelena T.
AU  - Novaković, Radmila
AU  - Đokić, Vladimir
AU  - Labudović-Borović, Milica
AU  - Tepavčević, Snežana
AU  - Zivanovic, Vladimir
AU  - Kanjuh, Vladimir
AU  - Heinle, Helmut
AU  - Gojković-Bukarica, Ljiljana
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7174
C3  - Atherosclerosis
T1  - Involvement of Atp-Sensitive Potassium Channels in Effect of Pinacidil on Saphenous Vein Obtained from the Patients with and Without Type 2 Diabetes Mellitus
VL  - 263
SP  - E131
EP  - E131
DO  - 10.1016/j.atherosclerosis.2017.06.418
ER  - 
@conference{
author = "Rajković, Jovana and Perić, Miodrag and Stanišić, Jelena and Rakočević, Jelena T. and Novaković, Radmila and Đokić, Vladimir and Labudović-Borović, Milica and Tepavčević, Snežana and Zivanovic, Vladimir and Kanjuh, Vladimir and Heinle, Helmut and Gojković-Bukarica, Ljiljana",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/7174",
journal = "Atherosclerosis",
title = "Involvement of Atp-Sensitive Potassium Channels in Effect of Pinacidil on Saphenous Vein Obtained from the Patients with and Without Type 2 Diabetes Mellitus",
volume = "263",
pages = "E131-E131",
doi = "10.1016/j.atherosclerosis.2017.06.418"
}
Rajković, J., Perić, M., Stanišić, J., Rakočević, J. T., Novaković, R., Đokić, V., Labudović-Borović, M., Tepavčević, S., Zivanovic, V., Kanjuh, V., Heinle, H.,& Gojković-Bukarica, L. (2017). Involvement of Atp-Sensitive Potassium Channels in Effect of Pinacidil on Saphenous Vein Obtained from the Patients with and Without Type 2 Diabetes Mellitus.
Atherosclerosis, 263, E131-E131.
https://doi.org/10.1016/j.atherosclerosis.2017.06.418
Rajković J, Perić M, Stanišić J, Rakočević JT, Novaković R, Đokić V, Labudović-Borović M, Tepavčević S, Zivanovic V, Kanjuh V, Heinle H, Gojković-Bukarica L. Involvement of Atp-Sensitive Potassium Channels in Effect of Pinacidil on Saphenous Vein Obtained from the Patients with and Without Type 2 Diabetes Mellitus. Atherosclerosis. 2017;263:E131-E131
Rajković Jovana, Perić Miodrag, Stanišić Jelena, Rakočević Jelena T., Novaković Radmila, Đokić Vladimir, Labudović-Borović Milica, Tepavčević Snežana, Zivanovic Vladimir, Kanjuh Vladimir, Heinle Helmut, Gojković-Bukarica Ljiljana, "Involvement of Atp-Sensitive Potassium Channels in Effect of Pinacidil on Saphenous Vein Obtained from the Patients with and Without Type 2 Diabetes Mellitus" Atherosclerosis, 263 (2017):E131-E131,
https://doi.org/10.1016/j.atherosclerosis.2017.06.418 .

Effect of Peroral Administration of Chromium on Insulin Signaling Pathway in Skeletal Muscle Tissue of Holstein Calves

Jovanović, Ljubomir J.; Pantelić, Marija; Prodanović, Radiša; Vujanac, Ivan; Đurić, Miloje; Tepavčević, Snežana; Vranješ-Đurić, Sanja; Korićanac, Goran; Kirovski, Danijela

(2017)

TY  - JOUR
AU  - Jovanović, Ljubomir J.
AU  - Pantelić, Marija
AU  - Prodanović, Radiša
AU  - Vujanac, Ivan
AU  - Đurić, Miloje
AU  - Tepavčević, Snežana
AU  - Vranješ-Đurić, Sanja
AU  - Korićanac, Goran
AU  - Kirovski, Danijela
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1808
AB  - The objective of this study was to investigate the effects of peroral administration of chromium-enriched yeast on glucose tolerance in Holstein calves, assessed by insulin signaling pathway molecule determination and intravenous glucose tolerance test (IVGTT). Twenty-four Holstein calves, aged 1 month, were chosen for the study and divided into two groups: the PoCr group (n = 12) that perorally received 0.04 mg of Cr/kg of body mass daily, for 70 days, and the NCr group (n = 12) that received no chromium supplementation. Skeletal tissue samples from each calf were obtained on day 0 and day 70 of the experiment. Chromium supplementation increased protein content of the insulin beta-subunit receptor, phosphorylation of insulin receptor substrate 1 at Tyrosine 632, phosphorylation of Akt at Serine 473, glucose transporter-4, and AMP-activated protein kinase in skeletal muscle tissue, while phosphorylation of insulin receptor substrate 1 at Serine 307 was not affected by chromium treatment. Results obtained during IVGTT, which was conducted on days 0, 30, 50, and 70, suggested an increased insulin sensitivity and, consequently, a better utilization of glucose in the PoCr group. Lower basal concentrations of glucose and insulin in the PoCr group on days 30 and 70 were also obtained. Our results indicate that chromium supplementation improves glucose utilization in calves by enhancing insulin intracellular signaling in the skeletal muscle tissue.
T2  - Biological Trace Element Research
T1  - Effect of Peroral Administration of Chromium on Insulin Signaling Pathway in Skeletal Muscle Tissue of Holstein Calves
VL  - 180
IS  - 2
SP  - 223
EP  - 232
DO  - 10.1007/s12011-017-1007-1
ER  - 
@article{
author = "Jovanović, Ljubomir J. and Pantelić, Marija and Prodanović, Radiša and Vujanac, Ivan and Đurić, Miloje and Tepavčević, Snežana and Vranješ-Đurić, Sanja and Korićanac, Goran and Kirovski, Danijela",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1808",
abstract = "The objective of this study was to investigate the effects of peroral administration of chromium-enriched yeast on glucose tolerance in Holstein calves, assessed by insulin signaling pathway molecule determination and intravenous glucose tolerance test (IVGTT). Twenty-four Holstein calves, aged 1 month, were chosen for the study and divided into two groups: the PoCr group (n = 12) that perorally received 0.04 mg of Cr/kg of body mass daily, for 70 days, and the NCr group (n = 12) that received no chromium supplementation. Skeletal tissue samples from each calf were obtained on day 0 and day 70 of the experiment. Chromium supplementation increased protein content of the insulin beta-subunit receptor, phosphorylation of insulin receptor substrate 1 at Tyrosine 632, phosphorylation of Akt at Serine 473, glucose transporter-4, and AMP-activated protein kinase in skeletal muscle tissue, while phosphorylation of insulin receptor substrate 1 at Serine 307 was not affected by chromium treatment. Results obtained during IVGTT, which was conducted on days 0, 30, 50, and 70, suggested an increased insulin sensitivity and, consequently, a better utilization of glucose in the PoCr group. Lower basal concentrations of glucose and insulin in the PoCr group on days 30 and 70 were also obtained. Our results indicate that chromium supplementation improves glucose utilization in calves by enhancing insulin intracellular signaling in the skeletal muscle tissue.",
journal = "Biological Trace Element Research",
title = "Effect of Peroral Administration of Chromium on Insulin Signaling Pathway in Skeletal Muscle Tissue of Holstein Calves",
volume = "180",
number = "2",
pages = "223-232",
doi = "10.1007/s12011-017-1007-1"
}
Jovanović, L. J., Pantelić, M., Prodanović, R., Vujanac, I., Đurić, M., Tepavčević, S., Vranješ-Đurić, S., Korićanac, G.,& Kirovski, D. (2017). Effect of Peroral Administration of Chromium on Insulin Signaling Pathway in Skeletal Muscle Tissue of Holstein Calves.
Biological Trace Element Research, 180(2), 223-232.
https://doi.org/10.1007/s12011-017-1007-1
Jovanović LJ, Pantelić M, Prodanović R, Vujanac I, Đurić M, Tepavčević S, Vranješ-Đurić S, Korićanac G, Kirovski D. Effect of Peroral Administration of Chromium on Insulin Signaling Pathway in Skeletal Muscle Tissue of Holstein Calves. Biological Trace Element Research. 2017;180(2):223-232
Jovanović Ljubomir J., Pantelić Marija, Prodanović Radiša, Vujanac Ivan, Đurić Miloje, Tepavčević Snežana, Vranješ-Đurić Sanja, Korićanac Goran, Kirovski Danijela, "Effect of Peroral Administration of Chromium on Insulin Signaling Pathway in Skeletal Muscle Tissue of Holstein Calves" Biological Trace Element Research, 180, no. 2 (2017):223-232,
https://doi.org/10.1007/s12011-017-1007-1 .
1
8
7
7

Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?

Bundalo, Maja M.; Romić, Snježana Đ.; Tepavčević, Snežana; Stojiljković, Mojca D.; Stanković, Aleksandra; Živković, Maja; Korićanac, Goran

(2017)

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Romić, Snježana Đ.
AU  - Tepavčević, Snežana
AU  - Stojiljković, Mojca D.
AU  - Stanković, Aleksandra
AU  - Živković, Maja
AU  - Korićanac, Goran
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1726
AB  - Increased intake of fructose in humans and laboratory animals is demonstrated to be a risk factor for development of metabolic disorders (insulin resistance, metabolic syndrome, type 2 diabetes) and cardiovascular diseases. On the other hand, estradiol is emphasized as a cardioprotective agent. The main goal of this review is to summarize recent findings on damaging cardiac effects of fructose-rich diet in females, mostly experimental animals, and to evaluate protective capacity of estradiol. Published results of our and other research groups indicate mostly detrimental effects of fructose-rich diet on cardiac insulin signaling molecules, glucose and fatty acid metabolism, nitric oxide production and ion transport, as well as renin-angiotensin system and inflammation. Some of these processes are involved in cardiac insulin signal transmission, others are regulated by insulin or have an influence on insulin action. Administration of estradiol to ovariectomized female rats, exposed to increased intake of fructose, was mostly beneficial to the heart, but sometimes it was ineffective or even detrimental, depending on the particular processes. We believe that these data, carefully translated to human population, could be useful for clinicians dealing with postmenopausal women susceptible to metabolic diseases and hormone replacement therapy.
T2  - European Journal of Pharmacology
T1  - Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?
VL  - 811
SP  - 141
EP  - 147
DO  - 10.1016/j.ejphar.2017.06.003
ER  - 
@article{
author = "Bundalo, Maja M. and Romić, Snježana Đ. and Tepavčević, Snežana and Stojiljković, Mojca D. and Stanković, Aleksandra and Živković, Maja and Korićanac, Goran",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1726",
abstract = "Increased intake of fructose in humans and laboratory animals is demonstrated to be a risk factor for development of metabolic disorders (insulin resistance, metabolic syndrome, type 2 diabetes) and cardiovascular diseases. On the other hand, estradiol is emphasized as a cardioprotective agent. The main goal of this review is to summarize recent findings on damaging cardiac effects of fructose-rich diet in females, mostly experimental animals, and to evaluate protective capacity of estradiol. Published results of our and other research groups indicate mostly detrimental effects of fructose-rich diet on cardiac insulin signaling molecules, glucose and fatty acid metabolism, nitric oxide production and ion transport, as well as renin-angiotensin system and inflammation. Some of these processes are involved in cardiac insulin signal transmission, others are regulated by insulin or have an influence on insulin action. Administration of estradiol to ovariectomized female rats, exposed to increased intake of fructose, was mostly beneficial to the heart, but sometimes it was ineffective or even detrimental, depending on the particular processes. We believe that these data, carefully translated to human population, could be useful for clinicians dealing with postmenopausal women susceptible to metabolic diseases and hormone replacement therapy.",
journal = "European Journal of Pharmacology",
title = "Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?",
volume = "811",
pages = "141-147",
doi = "10.1016/j.ejphar.2017.06.003"
}
Bundalo, M. M., Romić, S. Đ., Tepavčević, S., Stojiljković, M. D., Stanković, A., Živković, M.,& Korićanac, G. (2017). Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?.
European Journal of Pharmacology, 811, 141-147.
https://doi.org/10.1016/j.ejphar.2017.06.003
Bundalo MM, Romić SĐ, Tepavčević S, Stojiljković MD, Stanković A, Živković M, Korićanac G. Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?. European Journal of Pharmacology. 2017;811:141-147
Bundalo Maja M., Romić Snježana Đ., Tepavčević Snežana, Stojiljković Mojca D., Stanković Aleksandra, Živković Maja, Korićanac Goran, "Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?" European Journal of Pharmacology, 811 (2017):141-147,
https://doi.org/10.1016/j.ejphar.2017.06.003 .
1
4
4
4

Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet

Stanišić, Jelena; Korićanac, Goran; Ćulafić, Tijana; Romić, Snježana Đ.; Stojiljković, Mojca D.; Kostić, Milan; Pantelić, Marija; Tepavčević, Snežana

(2016)

TY  - JOUR
AU  - Stanišić, Jelena
AU  - Korićanac, Goran
AU  - Ćulafić, Tijana
AU  - Romić, Snježana Đ.
AU  - Stojiljković, Mojca D.
AU  - Kostić, Milan
AU  - Pantelić, Marija
AU  - Tepavčević, Snežana
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/913
AB  - Increase in fructose consumption together with decrease in physical activity contributes to the development of metabolic syndrome and consequently cardiovascular diseases. The current study examined the preventive role of exercise on defects in cardiac insulin signaling and function of endothelial nitric oxide synthase (eNOS) in fructose fed rats. Male Wistar rats were divided into control, sedentary fructose (received 10% fructose for 9 weeks) and exercise fructose (additionally exposed to low intensity exercise) groups. Concentration of triglycerides, glucose, insulin and visceral adipose tissue weight were determined to estimate metabolic syndrome development. Expression and/or phosphorylation of cardiac insulin receptor (IR), insulin receptor substrate 1 (IRS1), tyrosine-specific protein phosphatase 1B (PTP1B), Akt, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and eNOS were evaluated. Fructose overload increased visceral adipose tissue, insulin concentration and homeostasis model assessment index. Exercise managed to decrease visceral adiposity and insulin level and to increase insulin sensitivity. Fructose diet increased level of cardiac PTP1B and pIRS1 (Ser307), while levels of IR and ERK1/2, as well as pIRS1 (Tyr 632), pAkt (Ser473, Thr308) and pERK1/2 were decreased. These disturbances were accompanied by reduced phosphorylation of eNOS at Ser1177. Exercise managed to prevent most of the disturbances in insulin signaling caused by fructose diet (except phosphorylation of IRS1 at Tyr 632 and phosphorylation and protein expression of ERK1/2) and consequently restored function of eNOS. Low intensity exercise could be considered as efficient treatment of cardiac insulin resistance induced by fructose diet. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
T2  - Molecular and Cellular Endocrinology
T1  - Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet
VL  - 420
IS  - C
SP  - 97
EP  - 104
DO  - 10.1016/j.mce.2015.11.032
ER  - 
@article{
author = "Stanišić, Jelena and Korićanac, Goran and Ćulafić, Tijana and Romić, Snježana Đ. and Stojiljković, Mojca D. and Kostić, Milan and Pantelić, Marija and Tepavčević, Snežana",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/913",
abstract = "Increase in fructose consumption together with decrease in physical activity contributes to the development of metabolic syndrome and consequently cardiovascular diseases. The current study examined the preventive role of exercise on defects in cardiac insulin signaling and function of endothelial nitric oxide synthase (eNOS) in fructose fed rats. Male Wistar rats were divided into control, sedentary fructose (received 10% fructose for 9 weeks) and exercise fructose (additionally exposed to low intensity exercise) groups. Concentration of triglycerides, glucose, insulin and visceral adipose tissue weight were determined to estimate metabolic syndrome development. Expression and/or phosphorylation of cardiac insulin receptor (IR), insulin receptor substrate 1 (IRS1), tyrosine-specific protein phosphatase 1B (PTP1B), Akt, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and eNOS were evaluated. Fructose overload increased visceral adipose tissue, insulin concentration and homeostasis model assessment index. Exercise managed to decrease visceral adiposity and insulin level and to increase insulin sensitivity. Fructose diet increased level of cardiac PTP1B and pIRS1 (Ser307), while levels of IR and ERK1/2, as well as pIRS1 (Tyr 632), pAkt (Ser473, Thr308) and pERK1/2 were decreased. These disturbances were accompanied by reduced phosphorylation of eNOS at Ser1177. Exercise managed to prevent most of the disturbances in insulin signaling caused by fructose diet (except phosphorylation of IRS1 at Tyr 632 and phosphorylation and protein expression of ERK1/2) and consequently restored function of eNOS. Low intensity exercise could be considered as efficient treatment of cardiac insulin resistance induced by fructose diet. (C) 2015 Elsevier Ireland Ltd. All rights reserved.",
journal = "Molecular and Cellular Endocrinology",
title = "Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet",
volume = "420",
number = "C",
pages = "97-104",
doi = "10.1016/j.mce.2015.11.032"
}
Stanišić, J., Korićanac, G., Ćulafić, T., Romić, S. Đ., Stojiljković, M. D., Kostić, M., Pantelić, M.,& Tepavčević, S. (2016). Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet.
Molecular and Cellular Endocrinology, 420(C), 97-104.
https://doi.org/10.1016/j.mce.2015.11.032
Stanišić J, Korićanac G, Ćulafić T, Romić SĐ, Stojiljković MD, Kostić M, Pantelić M, Tepavčević S. Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet. Molecular and Cellular Endocrinology. 2016;420(C):97-104
Stanišić Jelena, Korićanac Goran, Ćulafić Tijana, Romić Snježana Đ., Stojiljković Mojca D., Kostić Milan, Pantelić Marija, Tepavčević Snežana, "Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet" Molecular and Cellular Endocrinology, 420, no. C (2016):97-104,
https://doi.org/10.1016/j.mce.2015.11.032 .
2
16
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11

Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta

Bundalo, Maja M.; Živković, Maja; Romić, Snježana Đ.; Tepavčević, Snežana; Korićanac, Goran; Đurić, Tamara; Stanković, Aleksandra

(2016)

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Živković, Maja
AU  - Romić, Snježana Đ.
AU  - Tepavčević, Snežana
AU  - Korićanac, Goran
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1132
AB  - Introduction: The cardiovascular renin-angiotensin system (RAS) could be affected by gender and dietary regime. We hypothesized that male rats will be more susceptible to activation of RAS in the heart and aorta, as a response to a fructose-rich diet (FRD). Materials and methods: Both male and female Wistar rats were given a 10% (w/v) fructose solution for 9 weeks. We measured the biochemical parameters, blood pressure (BP) and heart rate. We used Western blot and real-time polymerase chain reaction (PCR) to quantify protein and gene expression. Results: In the male rats, the FRD elevated BP and expression of cardiac angiotensin-converting enzyme (ACE), while the expression of angiotensin-converting enzyme 2 (ACE2) and angiotensin II Type 2 receptor (AT(2)R) were significantly decreased. In female rats, there were no changes in cardiac RAS expression due to FRD. Furthermore, the ACE/AT(1)R axis was overexpressed in the FRD male rats aortae, while only AT(1)R was upregulated in the FRD female rats aortae. ACE2 expression remained unchanged in the aortae of both genders receiving the FRD. Conclusions: The FRD induced gender-specific changes in the expression of the RAS in the heart and aortae of male rats. Further investigations are required in order to get a comprehensive understanding of the underlying mechanisms of gender-specific fructose-induced cardiovascular pathologies.
T2  - Journal of the Renin-Angiotensin-Aldosterone System
T1  - Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta
VL  - 17
IS  - 2
DO  - 10.1177/1470320316642915
ER  - 
@article{
author = "Bundalo, Maja M. and Živković, Maja and Romić, Snježana Đ. and Tepavčević, Snežana and Korićanac, Goran and Đurić, Tamara and Stanković, Aleksandra",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1132",
abstract = "Introduction: The cardiovascular renin-angiotensin system (RAS) could be affected by gender and dietary regime. We hypothesized that male rats will be more susceptible to activation of RAS in the heart and aorta, as a response to a fructose-rich diet (FRD). Materials and methods: Both male and female Wistar rats were given a 10% (w/v) fructose solution for 9 weeks. We measured the biochemical parameters, blood pressure (BP) and heart rate. We used Western blot and real-time polymerase chain reaction (PCR) to quantify protein and gene expression. Results: In the male rats, the FRD elevated BP and expression of cardiac angiotensin-converting enzyme (ACE), while the expression of angiotensin-converting enzyme 2 (ACE2) and angiotensin II Type 2 receptor (AT(2)R) were significantly decreased. In female rats, there were no changes in cardiac RAS expression due to FRD. Furthermore, the ACE/AT(1)R axis was overexpressed in the FRD male rats aortae, while only AT(1)R was upregulated in the FRD female rats aortae. ACE2 expression remained unchanged in the aortae of both genders receiving the FRD. Conclusions: The FRD induced gender-specific changes in the expression of the RAS in the heart and aortae of male rats. Further investigations are required in order to get a comprehensive understanding of the underlying mechanisms of gender-specific fructose-induced cardiovascular pathologies.",
journal = "Journal of the Renin-Angiotensin-Aldosterone System",
title = "Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta",
volume = "17",
number = "2",
doi = "10.1177/1470320316642915"
}
Bundalo, M. M., Živković, M., Romić, S. Đ., Tepavčević, S., Korićanac, G., Đurić, T.,& Stanković, A. (2016). Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta.
Journal of the Renin-Angiotensin-Aldosterone System, 17(2).
https://doi.org/10.1177/1470320316642915
Bundalo MM, Živković M, Romić SĐ, Tepavčević S, Korićanac G, Đurić T, Stanković A. Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta. Journal of the Renin-Angiotensin-Aldosterone System. 2016;17(2)
Bundalo Maja M., Živković Maja, Romić Snježana Đ., Tepavčević Snežana, Korićanac Goran, Đurić Tamara, Stanković Aleksandra, "Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta" Journal of the Renin-Angiotensin-Aldosterone System, 17, no. 2 (2016),
https://doi.org/10.1177/1470320316642915 .
17
14
16

Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome

Tepavčević, Snežana; Milutinovic, Danijela Vojnovic; Macut, Djuro; Stojiljković, Mojca D.; Nikolic, Marina; Bozic-Antic, Ivana; Ćulafić, Tijana; Bjekic-Macut, Jelica; Matić, Gordana; Korićanac, Goran

(2015)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, Danijela Vojnovic
AU  - Macut, Djuro
AU  - Stojiljković, Mojca D.
AU  - Nikolic, Marina
AU  - Bozic-Antic, Ivana
AU  - Ćulafić, Tijana
AU  - Bjekic-Macut, Jelica
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/710
AB  - Polycystic ovary syndrome (PCOS) is associated with an altered plasma lipid profile and increased risk for cardiovascular diseases. We hypothesized that molecular mechanisms underlying cardiac pathology in PCOS involve changes in expression and subcellular localization of several key proteins involved in cardiac lipid transport and metabolism, such as fatty acid transporter CD36, lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1), and carnitine palmitoyltransferase 1 (CPT1). We used the animal model of PCOS obtained by treating female rats with dihydrotestosterone (DHT). Protein levels of CD36, lipin 1, PPAR alpha, PGC1, and antioxidative enzymes were assessed by Western blot in different cardiac cell compartments. Cardiac triglycerides (TG) and lipid peroxidation were also measured. The content of CD36 was decreased in both the cardiac plasma membranes and intracellular pool. On the other hand, total content of cardiac lipin 1 in DHT-treated rats was elevated, in contrast to decreased microsomal lipin 1 content. An increase in nuclear content of lipin 1 was observed together with elevation of nuclear PPAR alpha and PGC1, and an increase in CPT1 expression. However, lipid peroxidation was reduced in the heart, without alterations in antioxidative enzymes expression and cardiac TG content. The results indicate that treatment of female rats with DHT is accompanied by a decrease of fatty acid uptake and a reduction of lipid peroxidation in the heart. The observed elevation of lipin 1, PPAR alpha, PGC1, and CPT1 expression suggests that cardiac fatty acid metabolism is shifted toward mitochondrial beta oxidation.
T2  - Endocrine
T1  - Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome
VL  - 50
IS  - 1
SP  - 193
EP  - 201
DO  - 10.1007/s12020-015-0558-1
ER  - 
@article{
author = "Tepavčević, Snežana and Milutinovic, Danijela Vojnovic and Macut, Djuro and Stojiljković, Mojca D. and Nikolic, Marina and Bozic-Antic, Ivana and Ćulafić, Tijana and Bjekic-Macut, Jelica and Matić, Gordana and Korićanac, Goran",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/710",
abstract = "Polycystic ovary syndrome (PCOS) is associated with an altered plasma lipid profile and increased risk for cardiovascular diseases. We hypothesized that molecular mechanisms underlying cardiac pathology in PCOS involve changes in expression and subcellular localization of several key proteins involved in cardiac lipid transport and metabolism, such as fatty acid transporter CD36, lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1), and carnitine palmitoyltransferase 1 (CPT1). We used the animal model of PCOS obtained by treating female rats with dihydrotestosterone (DHT). Protein levels of CD36, lipin 1, PPAR alpha, PGC1, and antioxidative enzymes were assessed by Western blot in different cardiac cell compartments. Cardiac triglycerides (TG) and lipid peroxidation were also measured. The content of CD36 was decreased in both the cardiac plasma membranes and intracellular pool. On the other hand, total content of cardiac lipin 1 in DHT-treated rats was elevated, in contrast to decreased microsomal lipin 1 content. An increase in nuclear content of lipin 1 was observed together with elevation of nuclear PPAR alpha and PGC1, and an increase in CPT1 expression. However, lipid peroxidation was reduced in the heart, without alterations in antioxidative enzymes expression and cardiac TG content. The results indicate that treatment of female rats with DHT is accompanied by a decrease of fatty acid uptake and a reduction of lipid peroxidation in the heart. The observed elevation of lipin 1, PPAR alpha, PGC1, and CPT1 expression suggests that cardiac fatty acid metabolism is shifted toward mitochondrial beta oxidation.",
journal = "Endocrine",
title = "Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome",
volume = "50",
number = "1",
pages = "193-201",
doi = "10.1007/s12020-015-0558-1"
}
Tepavčević, S., Milutinovic, D. V., Macut, D., Stojiljković, M. D., Nikolic, M., Bozic-Antic, I., Ćulafić, T., Bjekic-Macut, J., Matić, G.,& Korićanac, G. (2015). Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome.
Endocrine, 50(1), 193-201.
https://doi.org/10.1007/s12020-015-0558-1
Tepavčević S, Milutinovic DV, Macut D, Stojiljković MD, Nikolic M, Bozic-Antic I, Ćulafić T, Bjekic-Macut J, Matić G, Korićanac G. Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome. Endocrine. 2015;50(1):193-201
Tepavčević Snežana, Milutinovic Danijela Vojnovic, Macut Djuro, Stojiljković Mojca D., Nikolic Marina, Bozic-Antic Ivana, Ćulafić Tijana, Bjekic-Macut Jelica, Matić Gordana, Korićanac Goran, "Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome" Endocrine, 50, no. 1 (2015):193-201,
https://doi.org/10.1007/s12020-015-0558-1 .
6
4
3

Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol

Bundalo, Maja M.; Živković, Maja; Tepavčević, Snežana; Ćulafić, Tijana; Korićanac, Goran; Stanković, Aleksandra

(2015)

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Živković, Maja
AU  - Tepavčević, Snežana
AU  - Ćulafić, Tijana
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/570
AB  - The renin-angiotensin system has been implicated in the development of metabolic syndrome and appears to be a key in the local tissue control of normal cardiac functions. Physiological concentrations of estrogens have been shown to be cardioprotective, especially against the damaging effects of fructose-rich diet. The aim of the study was to investigate the expression of the renin-angiotensin system molecules with potentially deleterious effect on the heart (angiotensin-converting enzyme and angiotensin II type 1 receptor) and those with potentially protective effects, (angiotensin-converting enzyme 2 and angiotensin II type 2 receptor), in ovariectomized fructose fed female rats with 17-estradiol replacement. Real-time PCR and Western blot analysis were used for quantification of gene and protein expression in the heart. Fructose diet increased the expression of angiotensin-converting enzyme and angiotensin II type 1 receptor and decreased the expression of angiotensin-converting enzyme 2 and angiotensin II type 2 receptor. On the other hand, estradiol replacement seems to undo fructose diet effects on cardiac renin-angiotensin system. Downregulation of angiotensin-converting enzyme and angiotensin II type 1 receptor, and reversion of expression of both potentially protective molecules, angiotensin-converting enzyme 2 and angiotensin II type 2 receptor, to the control level in cardiac tissue took place. Obtained results suggest that estradiol may reverse the harmful effect of fructose-rich diet on the expression of renin-angiotensin system molecules. These findings may also be important in further research of phenotypes like insulin resistance, metabolic syndrome, and following cardiovascular pathology in females.
T2  - Hormone and Metabolic Research
T1  - Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol
VL  - 47
IS  - 7
SP  - 521
EP  - 527
DO  - 10.1055/s-0034-1394373
ER  - 
@article{
author = "Bundalo, Maja M. and Živković, Maja and Tepavčević, Snežana and Ćulafić, Tijana and Korićanac, Goran and Stanković, Aleksandra",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/570",
abstract = "The renin-angiotensin system has been implicated in the development of metabolic syndrome and appears to be a key in the local tissue control of normal cardiac functions. Physiological concentrations of estrogens have been shown to be cardioprotective, especially against the damaging effects of fructose-rich diet. The aim of the study was to investigate the expression of the renin-angiotensin system molecules with potentially deleterious effect on the heart (angiotensin-converting enzyme and angiotensin II type 1 receptor) and those with potentially protective effects, (angiotensin-converting enzyme 2 and angiotensin II type 2 receptor), in ovariectomized fructose fed female rats with 17-estradiol replacement. Real-time PCR and Western blot analysis were used for quantification of gene and protein expression in the heart. Fructose diet increased the expression of angiotensin-converting enzyme and angiotensin II type 1 receptor and decreased the expression of angiotensin-converting enzyme 2 and angiotensin II type 2 receptor. On the other hand, estradiol replacement seems to undo fructose diet effects on cardiac renin-angiotensin system. Downregulation of angiotensin-converting enzyme and angiotensin II type 1 receptor, and reversion of expression of both potentially protective molecules, angiotensin-converting enzyme 2 and angiotensin II type 2 receptor, to the control level in cardiac tissue took place. Obtained results suggest that estradiol may reverse the harmful effect of fructose-rich diet on the expression of renin-angiotensin system molecules. These findings may also be important in further research of phenotypes like insulin resistance, metabolic syndrome, and following cardiovascular pathology in females.",
journal = "Hormone and Metabolic Research",
title = "Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol",
volume = "47",
number = "7",
pages = "521-527",
doi = "10.1055/s-0034-1394373"
}
Bundalo, M. M., Živković, M., Tepavčević, S., Ćulafić, T., Korićanac, G.,& Stanković, A. (2015). Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol.
Hormone and Metabolic Research, 47(7), 521-527.
https://doi.org/10.1055/s-0034-1394373
Bundalo MM, Živković M, Tepavčević S, Ćulafić T, Korićanac G, Stanković A. Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol. Hormone and Metabolic Research. 2015;47(7):521-527
Bundalo Maja M., Živković Maja, Tepavčević Snežana, Ćulafić Tijana, Korićanac Goran, Stanković Aleksandra, "Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol" Hormone and Metabolic Research, 47, no. 7 (2015):521-527,
https://doi.org/10.1055/s-0034-1394373 .
8
8
8

Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone

Tepavčević, Snežana; Milutinovic, D. V.; Macut, D.; Stanišić, Jelena; Nikolic, M.; Bozic-Antic, I.; Rodaljevic, S.; Bjekic-Macut, J.; Matić, Gordana; Korićanac, Goran

(2015)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, D. V.
AU  - Macut, D.
AU  - Stanišić, Jelena
AU  - Nikolic, M.
AU  - Bozic-Antic, I.
AU  - Rodaljevic, S.
AU  - Bjekic-Macut, J.
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/553
AB  - Nitric oxide synthases (NOSs) and Na+/K+-ATPase are enzymes essential for regular functioning of the heart. Since both enzymes are under insulin and androgen regulation and since insulin action and androgen level were disturbed in polycystic ovary syndrome (PCOS), we hypothesized that cardiac nitric oxide (NO) production and sodium/potassium transport would be deteriorated in PCOS. To test our hypothesis we introduced animal model of PCOS based on dihydrotestosterone (DHT) treatment of female Wistar rats and analyzed protein expression, phosphorylation or subcellular localization of endothelial NOS (eNOS), inducible NOS (iNOS) and alpha subunits of Na+/K+-ATPase in the heart. Obtained results indicate that DHT treatment significantly decreased cardiac eNOS protein level and activating phosphorylation at serine 1177, while inhibitory phosphorylation at threonine 495 was increased. In contrast to expression of eNOS, iNOS protein level in the heart of DHT-treated rats was significantly elevated. Furthermore, cardiac protein level of alpha 1 subunit of the ATPase, as well as its plasma membrane content, were decreased in rats with PCOS. In line with this, alpha 2 subunit protein level in fraction of plasma membranes was also significantly below control level. In conclusion, DHT treatment impaired effectiveness of NOSs and Na+/K+-ATPase in the female rat heart. Regarding the importance of NO production and sodium/potassium transport in the cardiac contraction and blood flow regulation, it implicates strong consequences of PCOS for heart functioning.
T2  - Experimental and Clinical Endocrinology and Diabetes
T1  - Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone
VL  - 123
IS  - 5
SP  - 303
EP  - 307
DO  - 10.1055/s-0035-1548929
ER  - 
@article{
author = "Tepavčević, Snežana and Milutinovic, D. V. and Macut, D. and Stanišić, Jelena and Nikolic, M. and Bozic-Antic, I. and Rodaljevic, S. and Bjekic-Macut, J. and Matić, Gordana and Korićanac, Goran",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/553",
abstract = "Nitric oxide synthases (NOSs) and Na+/K+-ATPase are enzymes essential for regular functioning of the heart. Since both enzymes are under insulin and androgen regulation and since insulin action and androgen level were disturbed in polycystic ovary syndrome (PCOS), we hypothesized that cardiac nitric oxide (NO) production and sodium/potassium transport would be deteriorated in PCOS. To test our hypothesis we introduced animal model of PCOS based on dihydrotestosterone (DHT) treatment of female Wistar rats and analyzed protein expression, phosphorylation or subcellular localization of endothelial NOS (eNOS), inducible NOS (iNOS) and alpha subunits of Na+/K+-ATPase in the heart. Obtained results indicate that DHT treatment significantly decreased cardiac eNOS protein level and activating phosphorylation at serine 1177, while inhibitory phosphorylation at threonine 495 was increased. In contrast to expression of eNOS, iNOS protein level in the heart of DHT-treated rats was significantly elevated. Furthermore, cardiac protein level of alpha 1 subunit of the ATPase, as well as its plasma membrane content, were decreased in rats with PCOS. In line with this, alpha 2 subunit protein level in fraction of plasma membranes was also significantly below control level. In conclusion, DHT treatment impaired effectiveness of NOSs and Na+/K+-ATPase in the female rat heart. Regarding the importance of NO production and sodium/potassium transport in the cardiac contraction and blood flow regulation, it implicates strong consequences of PCOS for heart functioning.",
journal = "Experimental and Clinical Endocrinology and Diabetes",
title = "Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone",
volume = "123",
number = "5",
pages = "303-307",
doi = "10.1055/s-0035-1548929"
}
Tepavčević, S., Milutinovic, D. V., Macut, D., Stanišić, J., Nikolic, M., Bozic-Antic, I., Rodaljevic, S., Bjekic-Macut, J., Matić, G.,& Korićanac, G. (2015). Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone.
Experimental and Clinical Endocrinology and Diabetes, 123(5), 303-307.
https://doi.org/10.1055/s-0035-1548929
Tepavčević S, Milutinovic DV, Macut D, Stanišić J, Nikolic M, Bozic-Antic I, Rodaljevic S, Bjekic-Macut J, Matić G, Korićanac G. Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone. Experimental and Clinical Endocrinology and Diabetes. 2015;123(5):303-307
Tepavčević Snežana, Milutinovic D. V., Macut D., Stanišić Jelena, Nikolic M., Bozic-Antic I., Rodaljevic S., Bjekic-Macut J., Matić Gordana, Korićanac Goran, "Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone" Experimental and Clinical Endocrinology and Diabetes, 123, no. 5 (2015):303-307,
https://doi.org/10.1055/s-0035-1548929 .
5
3
4

Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats

Romić, Snježana Đ.; Tepavčević, Snežana; Žakula, Zorica; Milosavljević, Tijana; Kostić, Milan; Petković, Marijana; Korićanac, Goran

(2014)

TY  - JOUR
AU  - Romić, Snježana Đ.
AU  - Tepavčević, Snežana
AU  - Žakula, Zorica
AU  - Milosavljević, Tijana
AU  - Kostić, Milan
AU  - Petković, Marijana
AU  - Korićanac, Goran
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/6053
AB  - To give new insight to alterations of cardiac lipid metabolism accompanied by a fructose-rich diet (FRD), rats of both sexes were exposed to 10 % fructose in drinking water during 9 weeks. The protein level and subcellular localization of the main regulators of cardiac lipid metabolism, such as lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha), carnitine palmitoyltransferase I (CPTI), and CD36 were studied. Caloric intake in fructose-fed rats (FFR) of both sexes was increased. Circulating triacylglyceroles (TAG) and non-esterified fatty acids were increased in male FFR, while females increased visceral adiposity and blood TAG. Total expression of lipin 1 in cardiac cell lysate and its cytosolic and microsomal level were increased in the hearts of male FFR. PPAR alpha and PGC-1 alpha content were decreased in the nuclear extract. In addition, cardiac deposition of TAG in male FFR was elevated, as well as inhibitory phosphorylation of insulin receptor substrate 1 (IRS-1). In contrast, in female FFR, lipin 1 level was increased in nuclear extract only, while overall CPTI expression and phosphorylation of IRS-1 at serine 307 were decreased. The results of our study suggest that fructose diet causes gender-dependent alterations in cardiac lipid metabolism. Potentially detrimental effects of FRD seem to be limited to male rats. Most of the observed changes might be a consequence of elevated expression and altered localization of lipin 1. Increased inhibitory phosphorylation of IRS-1 is possible link between cardiac lipid metabolism and insulin resistance in FFR.
T2  - Lipids
T1  - Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats
VL  - 49
IS  - 7
SP  - 655
EP  - 663
DO  - 10.1007/s11745-014-3909-4
ER  - 
@article{
author = "Romić, Snježana Đ. and Tepavčević, Snežana and Žakula, Zorica and Milosavljević, Tijana and Kostić, Milan and Petković, Marijana and Korićanac, Goran",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/6053",
abstract = "To give new insight to alterations of cardiac lipid metabolism accompanied by a fructose-rich diet (FRD), rats of both sexes were exposed to 10 % fructose in drinking water during 9 weeks. The protein level and subcellular localization of the main regulators of cardiac lipid metabolism, such as lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha), carnitine palmitoyltransferase I (CPTI), and CD36 were studied. Caloric intake in fructose-fed rats (FFR) of both sexes was increased. Circulating triacylglyceroles (TAG) and non-esterified fatty acids were increased in male FFR, while females increased visceral adiposity and blood TAG. Total expression of lipin 1 in cardiac cell lysate and its cytosolic and microsomal level were increased in the hearts of male FFR. PPAR alpha and PGC-1 alpha content were decreased in the nuclear extract. In addition, cardiac deposition of TAG in male FFR was elevated, as well as inhibitory phosphorylation of insulin receptor substrate 1 (IRS-1). In contrast, in female FFR, lipin 1 level was increased in nuclear extract only, while overall CPTI expression and phosphorylation of IRS-1 at serine 307 were decreased. The results of our study suggest that fructose diet causes gender-dependent alterations in cardiac lipid metabolism. Potentially detrimental effects of FRD seem to be limited to male rats. Most of the observed changes might be a consequence of elevated expression and altered localization of lipin 1. Increased inhibitory phosphorylation of IRS-1 is possible link between cardiac lipid metabolism and insulin resistance in FFR.",
journal = "Lipids",
title = "Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats",
volume = "49",
number = "7",
pages = "655-663",
doi = "10.1007/s11745-014-3909-4"
}
Romić, S. Đ., Tepavčević, S., Žakula, Z., Milosavljević, T., Kostić, M., Petković, M.,& Korićanac, G. (2014). Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats.
Lipids, 49(7), 655-663.
https://doi.org/10.1007/s11745-014-3909-4
Romić SĐ, Tepavčević S, Žakula Z, Milosavljević T, Kostić M, Petković M, Korićanac G. Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats. Lipids. 2014;49(7):655-663
Romić Snježana Đ., Tepavčević Snežana, Žakula Zorica, Milosavljević Tijana, Kostić Milan, Petković Marijana, Korićanac Goran, "Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats" Lipids, 49, no. 7 (2014):655-663,
https://doi.org/10.1007/s11745-014-3909-4 .
5
5
5

Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol

Korićanac, Goran; Tepavčević, Snežana; Romić, Snježana Đ.; Milosavljević, Tijana; Stojiljković, Mojca D.; Žakula, Zorica

(2014)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Romić, Snježana Đ.
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Žakula, Zorica
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5879
T2  - Hormone and Metabolic Research
T1  - Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol
VL  - 46
IS  - 2
SP  - 109
EP  - 115
ER  - 
@article{
author = "Korićanac, Goran and Tepavčević, Snežana and Romić, Snježana Đ. and Milosavljević, Tijana and Stojiljković, Mojca D. and Žakula, Zorica",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5879",
journal = "Hormone and Metabolic Research",
title = "Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol",
volume = "46",
number = "2",
pages = "109-115"
}
Korićanac, G., Tepavčević, S., Romić, S. Đ., Milosavljević, T., Stojiljković, M. D.,& Žakula, Z. (2014). Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol.
Hormone and Metabolic Research, 46(2), 109-115.
Korićanac G, Tepavčević S, Romić SĐ, Milosavljević T, Stojiljković MD, Žakula Z. Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol. Hormone and Metabolic Research. 2014;46(2):109-115
Korićanac Goran, Tepavčević Snežana, Romić Snježana Đ., Milosavljević Tijana, Stojiljković Mojca D., Žakula Zorica, "Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol" Hormone and Metabolic Research, 46, no. 2 (2014):109-115
7

Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome

Tepavčević, Snežana; Milutinovic, Danijela Vojnovic; Macut, Djuro; Žakula, Zorica; Nikolic, Marina; Bozic-Antic, Ivana; Romić, Snježana Đ.; Bjekic-Macut, Jelica; Matić, Gordana; Korićanac, Goran

(2014)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, Danijela Vojnovic
AU  - Macut, Djuro
AU  - Žakula, Zorica
AU  - Nikolic, Marina
AU  - Bozic-Antic, Ivana
AU  - Romić, Snježana Đ.
AU  - Bjekic-Macut, Jelica
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5970
AB  - It is supposed that women with polycystic ovary syndrome (PCOS) are prone to develop cardiovascular disease as a consequence of multiple risk factors that are mostly related to the state of insulin resistance and consequent hyperinsulinemia. In the present study, we evaluated insulin signaling and glucose transporters (GLUT) in cardiac cells of dihydrotestosterone (DHT) treated female rats as an animal model of PCOS. Expression of proteins involved in cardiac insulin signaling pathways and glucose transporters, as well as their phosphorylation or intracellular localization were studied by Western blot analysis in DHT-treated and control rats. Treatment with DHT resulted in increased body mass, absolute mass of the heart, elevated plasma insulin concentration, dyslipidemia and insulin resistance. At the molecular level, DHT treatment did not change protein expression of cardiac insulin receptor and insulin receptor substrate 1, while phosphorylation of the substrate at serine 307 was increased. Unexpectedly, although expression of downstream Akt kinase and its phosphorylation at threonine 308 were not altered, phosphoiylation of Akt at serine 473 was increased in the heart of DHT-treated rats. In contrast, expression and phosphorylation of extracellular signal regulated kinases 1/2 were decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased, as well as the expression of GLUT4 in cardiac cells at the end of androgen treatment. The obtained results provide evidence for alterations in expression and especially in functional characteristics of insulin signaling molecules and glucose transporters in the heart of DHT-treated rats with PCOS, indicating impaired cardiac insulin action. (c) 2014 Elsevier Ltd. All rights reserved.
T2  - Journal of Steroid Biochemistry and Molecular Biology
T1  - Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome
VL  - 141
SP  - 71
EP  - 76
DO  - 10.1016/j.jsbmb.2014.01.006
ER  - 
@article{
author = "Tepavčević, Snežana and Milutinovic, Danijela Vojnovic and Macut, Djuro and Žakula, Zorica and Nikolic, Marina and Bozic-Antic, Ivana and Romić, Snježana Đ. and Bjekic-Macut, Jelica and Matić, Gordana and Korićanac, Goran",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5970",
abstract = "It is supposed that women with polycystic ovary syndrome (PCOS) are prone to develop cardiovascular disease as a consequence of multiple risk factors that are mostly related to the state of insulin resistance and consequent hyperinsulinemia. In the present study, we evaluated insulin signaling and glucose transporters (GLUT) in cardiac cells of dihydrotestosterone (DHT) treated female rats as an animal model of PCOS. Expression of proteins involved in cardiac insulin signaling pathways and glucose transporters, as well as their phosphorylation or intracellular localization were studied by Western blot analysis in DHT-treated and control rats. Treatment with DHT resulted in increased body mass, absolute mass of the heart, elevated plasma insulin concentration, dyslipidemia and insulin resistance. At the molecular level, DHT treatment did not change protein expression of cardiac insulin receptor and insulin receptor substrate 1, while phosphorylation of the substrate at serine 307 was increased. Unexpectedly, although expression of downstream Akt kinase and its phosphorylation at threonine 308 were not altered, phosphoiylation of Akt at serine 473 was increased in the heart of DHT-treated rats. In contrast, expression and phosphorylation of extracellular signal regulated kinases 1/2 were decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased, as well as the expression of GLUT4 in cardiac cells at the end of androgen treatment. The obtained results provide evidence for alterations in expression and especially in functional characteristics of insulin signaling molecules and glucose transporters in the heart of DHT-treated rats with PCOS, indicating impaired cardiac insulin action. (c) 2014 Elsevier Ltd. All rights reserved.",
journal = "Journal of Steroid Biochemistry and Molecular Biology",
title = "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome",
volume = "141",
pages = "71-76",
doi = "10.1016/j.jsbmb.2014.01.006"
}
Tepavčević, S., Milutinovic, D. V., Macut, D., Žakula, Z., Nikolic, M., Bozic-Antic, I., Romić, S. Đ., Bjekic-Macut, J., Matić, G.,& Korićanac, G. (2014). Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome.
Journal of Steroid Biochemistry and Molecular Biology, 141, 71-76.
https://doi.org/10.1016/j.jsbmb.2014.01.006
Tepavčević S, Milutinovic DV, Macut D, Žakula Z, Nikolic M, Bozic-Antic I, Romić SĐ, Bjekic-Macut J, Matić G, Korićanac G. Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome. Journal of Steroid Biochemistry and Molecular Biology. 2014;141:71-76
Tepavčević Snežana, Milutinovic Danijela Vojnovic, Macut Djuro, Žakula Zorica, Nikolic Marina, Bozic-Antic Ivana, Romić Snježana Đ., Bjekic-Macut Jelica, Matić Gordana, Korićanac Goran, "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome" Journal of Steroid Biochemistry and Molecular Biology, 141 (2014):71-76,
https://doi.org/10.1016/j.jsbmb.2014.01.006 .
12
11
12

Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver

Dobutovic, Branislava; Sudar, Emina; Tepavčević, Snežana; Đorđević, Jelena D.; Đorđević, Ana D.; Radoičić, Marija B.; Isenović, Esma R.

(2014)

TY  - JOUR
AU  - Dobutovic, Branislava
AU  - Sudar, Emina
AU  - Tepavčević, Snežana
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Radoičić, Marija B.
AU  - Isenović, Esma R.
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/93
AB  - Introduction: We investigated the effects of ghrelin on protein expression of the liver antioxidant enzymes superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), nuclear factor kappa B (NF kappa B) and inducible nitric oxide synthase (iNOS). Furthermore, we aimed to investigate whether extracellular regulated protein kinase (ERK1/2) and protein kinase B (Akt) are involved in ghrelin-regulated liver antioxidant enzymes and iNOS protein expression. Material and methods: Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) injected into the lateral cerebral ventricle every 24 h for 5 days, and 2 h after the last treatment the animals were sacrificed and the liver excised. The Western blot method was used to determine expression of antioxidant enzymes, iNOS, phosphorylation of Akt, ERK1/2 and nuclear factor kappa B (NF kappa B) subunits 50 and 65. Results: There was significantly higher protein expression of CuZnSOD (p LT 0.001), MnSOD (p LT 0.001), CAT (p LT 0.001), GPx, (p LT 0.001), and GR (p LT 0.01) in the liver isolated from ghrelin-treated animals compared with control animals. In contrast, ghrelin significantly (p LT 0.01) reduced protein expression of iNOS. In addition, phosphorylation of NF kappa B subunits p65 and p50 was significantly (p LT 0.001 for p65; p LT 0.05 for p50) reduced by ghrelin when compared with controls. Phosphorylation of ERK1/2 and of Akt was significantly higher in ghrelin-treated than in control animals (p LT 0.05 for ERK1/2; p LT 0.01 for Akt). Conclusions: The results show that activation of Akt and ERK1/2 is involved in ghrelin-mediated regulation of protein expression of antioxidant enzymes and iNOS in the rat liver.
T2  - Archives of Medical Science
T1  - Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver
VL  - 10
IS  - 4
SP  - 806
EP  - 816
DO  - 10.5114/aoms.2014.44872
ER  - 
@article{
author = "Dobutovic, Branislava and Sudar, Emina and Tepavčević, Snežana and Đorđević, Jelena D. and Đorđević, Ana D. and Radoičić, Marija B. and Isenović, Esma R.",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/93",
abstract = "Introduction: We investigated the effects of ghrelin on protein expression of the liver antioxidant enzymes superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), nuclear factor kappa B (NF kappa B) and inducible nitric oxide synthase (iNOS). Furthermore, we aimed to investigate whether extracellular regulated protein kinase (ERK1/2) and protein kinase B (Akt) are involved in ghrelin-regulated liver antioxidant enzymes and iNOS protein expression. Material and methods: Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) injected into the lateral cerebral ventricle every 24 h for 5 days, and 2 h after the last treatment the animals were sacrificed and the liver excised. The Western blot method was used to determine expression of antioxidant enzymes, iNOS, phosphorylation of Akt, ERK1/2 and nuclear factor kappa B (NF kappa B) subunits 50 and 65. Results: There was significantly higher protein expression of CuZnSOD (p LT 0.001), MnSOD (p LT 0.001), CAT (p LT 0.001), GPx, (p LT 0.001), and GR (p LT 0.01) in the liver isolated from ghrelin-treated animals compared with control animals. In contrast, ghrelin significantly (p LT 0.01) reduced protein expression of iNOS. In addition, phosphorylation of NF kappa B subunits p65 and p50 was significantly (p LT 0.001 for p65; p LT 0.05 for p50) reduced by ghrelin when compared with controls. Phosphorylation of ERK1/2 and of Akt was significantly higher in ghrelin-treated than in control animals (p LT 0.05 for ERK1/2; p LT 0.01 for Akt). Conclusions: The results show that activation of Akt and ERK1/2 is involved in ghrelin-mediated regulation of protein expression of antioxidant enzymes and iNOS in the rat liver.",
journal = "Archives of Medical Science",
title = "Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver",
volume = "10",
number = "4",
pages = "806-816",
doi = "10.5114/aoms.2014.44872"
}
Dobutovic, B., Sudar, E., Tepavčević, S., Đorđević, J. D., Đorđević, A. D., Radoičić, M. B.,& Isenović, E. R. (2014). Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver.
Archives of Medical Science, 10(4), 806-816.
https://doi.org/10.5114/aoms.2014.44872
Dobutovic B, Sudar E, Tepavčević S, Đorđević JD, Đorđević AD, Radoičić MB, Isenović ER. Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver. Archives of Medical Science. 2014;10(4):806-816
Dobutovic Branislava, Sudar Emina, Tepavčević Snežana, Đorđević Jelena D., Đorđević Ana D., Radoičić Marija B., Isenović Esma R., "Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver" Archives of Medical Science, 10, no. 4 (2014):806-816,
https://doi.org/10.5114/aoms.2014.44872 .
18
17
22

Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats

Korićanac, Goran; Đorđević, Ana D.; Žakula, Zorica; Vojnovic-Milutinovic, Danijela; Tepavčević, Snežana; Velikovic, Natasa; Milosavljević, Tijana; Stojiljković, Mojca D.; Romić, Snježana Đ.; Matić, Gordana

(2013)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Đorđević, Ana D.
AU  - Žakula, Zorica
AU  - Vojnovic-Milutinovic, Danijela
AU  - Tepavčević, Snežana
AU  - Velikovic, Natasa
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Romić, Snježana Đ.
AU  - Matić, Gordana
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5507
AB  - We analyzed the effects of a fructose-rich diet (FRD) to test the assumption that the expression of metabolic syndrome phenotype is different in male and female rats. Two-way ANOVA revealed a significant effect of FRD on feeding behavior and carbohydrate/lipid metabolism. The increased caloric intake in FRD rats of both sexes was followed by a cluster of gender-specific changes typical for the metabolic syndrome. Female rats were characterized by decreased glycemia, increased triglycerides, enlarged visceral adipose tissue and increased absolute mass of liver, without changes in systolic blood pressure and insulin sensitivity. In contrast, male rats developed less disturbances in physical and biochemical characteristics, but blood pressure and insulin sensitivity were impaired by FRD. The results emphasize the detrimental effects of fructose consumption on cardiovascular risk and insulin action in males, whereas females are affected by other metabolic disturbances. These results support the idea of gender-dependent differences in the expression of the metabolic syndrome phenotype.
T2  - Archives of biological sciences
T1  - Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats
VL  - 65
IS  - 2
SP  - 455
EP  - 464
DO  - 10.2298/ABS1302455K
ER  - 
@article{
author = "Korićanac, Goran and Đorđević, Ana D. and Žakula, Zorica and Vojnovic-Milutinovic, Danijela and Tepavčević, Snežana and Velikovic, Natasa and Milosavljević, Tijana and Stojiljković, Mojca D. and Romić, Snježana Đ. and Matić, Gordana",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5507",
abstract = "We analyzed the effects of a fructose-rich diet (FRD) to test the assumption that the expression of metabolic syndrome phenotype is different in male and female rats. Two-way ANOVA revealed a significant effect of FRD on feeding behavior and carbohydrate/lipid metabolism. The increased caloric intake in FRD rats of both sexes was followed by a cluster of gender-specific changes typical for the metabolic syndrome. Female rats were characterized by decreased glycemia, increased triglycerides, enlarged visceral adipose tissue and increased absolute mass of liver, without changes in systolic blood pressure and insulin sensitivity. In contrast, male rats developed less disturbances in physical and biochemical characteristics, but blood pressure and insulin sensitivity were impaired by FRD. The results emphasize the detrimental effects of fructose consumption on cardiovascular risk and insulin action in males, whereas females are affected by other metabolic disturbances. These results support the idea of gender-dependent differences in the expression of the metabolic syndrome phenotype.",
journal = "Archives of biological sciences",
title = "Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats",
volume = "65",
number = "2",
pages = "455-464",
doi = "10.2298/ABS1302455K"
}
Korićanac, G., Đorđević, A. D., Žakula, Z., Vojnovic-Milutinovic, D., Tepavčević, S., Velikovic, N., Milosavljević, T., Stojiljković, M. D., Romić, S. Đ.,& Matić, G. (2013). Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats.
Archives of biological sciences, 65(2), 455-464.
https://doi.org/10.2298/ABS1302455K
Korićanac G, Đorđević AD, Žakula Z, Vojnovic-Milutinovic D, Tepavčević S, Velikovic N, Milosavljević T, Stojiljković MD, Romić SĐ, Matić G. Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats. Archives of biological sciences. 2013;65(2):455-464
Korićanac Goran, Đorđević Ana D., Žakula Zorica, Vojnovic-Milutinovic Danijela, Tepavčević Snežana, Velikovic Natasa, Milosavljević Tijana, Stojiljković Mojca D., Romić Snježana Đ., Matić Gordana, "Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats" Archives of biological sciences, 65, no. 2 (2013):455-464,
https://doi.org/10.2298/ABS1302455K .
12
12
12

Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?

Romić, Snježana Đ.; Tepavčević, Snežana; Žakula, Zorica; Milosavljević, Tijana; Stojiljković, Mojca D.; Živković, Maja; Popović, Milan; Stanković, Aleksandra; Korićanac, Goran

(2013)

TY  - JOUR
AU  - Romić, Snježana Đ.
AU  - Tepavčević, Snežana
AU  - Žakula, Zorica
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Živković, Maja
AU  - Popović, Milan
AU  - Stanković, Aleksandra
AU  - Korićanac, Goran
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5513
AB  - Fructose-rich diets (FRD) cause cardiac insulin resistance manifested by impairment of Akt/endothelial NO synthase (eNOS) signalling. In contrast, oestradiol (E2) activates this signalling pathway in the heart. To study the ability of E2 to revert the detrimental effect of fructose on cardiac Akt/eNOS, female rats were subjected to a FRD and ovariectomy followed with or without E2 replacement. We also analysed the effects of the FRD and E2 on cardiac extracellular signal-regulated kinase (Erk 1/2) signalling related to their role in cardiac hypertrophy development. Expression of Akt, eNOS and Erk 1/2, as well as regulatory phosphorylations of these molecules were determined. The protein expression of cardiac Akt and eNOS was not affected by the diet or E2 treatment. However, the FRD was accompanied by a decrease in Akt phosphorylation at Ser(473) and Thr(308), and eNOS at Ser(1177), while the phosphorylation of eNOS at Thr(495) was increased. E2 replacement in ovariectomised fructose-fed rats caused a reversion of the diet effect on Akt and eNOS serine phosphorylation, but mostly had no effect on threonine phosphorylation of the molecules. The FRD and E2 treatment did not influence Erk 1/2 expression and phosphorylation and heart mass as well. The data show that E2 selectively suppress the negative effects of a FRD on Akt/eNOS signalling and probably point to the different effects of E2 on kinase/phosphatase pathways responsible for phosphorylation/dephosphorylation of Akt and eNOS. Furthermore, the results suggest that the heart of females in the reproductive period is partially protected against the damaging effects of increased fructose intake.
T2  - British Journal of Nutrition
T1  - Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?
VL  - 109
IS  - 11
SP  - 1940
EP  - 1948
DO  - 10.1017/S0007114512004114
ER  - 
@article{
author = "Romić, Snježana Đ. and Tepavčević, Snežana and Žakula, Zorica and Milosavljević, Tijana and Stojiljković, Mojca D. and Živković, Maja and Popović, Milan and Stanković, Aleksandra and Korićanac, Goran",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5513",
abstract = "Fructose-rich diets (FRD) cause cardiac insulin resistance manifested by impairment of Akt/endothelial NO synthase (eNOS) signalling. In contrast, oestradiol (E2) activates this signalling pathway in the heart. To study the ability of E2 to revert the detrimental effect of fructose on cardiac Akt/eNOS, female rats were subjected to a FRD and ovariectomy followed with or without E2 replacement. We also analysed the effects of the FRD and E2 on cardiac extracellular signal-regulated kinase (Erk 1/2) signalling related to their role in cardiac hypertrophy development. Expression of Akt, eNOS and Erk 1/2, as well as regulatory phosphorylations of these molecules were determined. The protein expression of cardiac Akt and eNOS was not affected by the diet or E2 treatment. However, the FRD was accompanied by a decrease in Akt phosphorylation at Ser(473) and Thr(308), and eNOS at Ser(1177), while the phosphorylation of eNOS at Thr(495) was increased. E2 replacement in ovariectomised fructose-fed rats caused a reversion of the diet effect on Akt and eNOS serine phosphorylation, but mostly had no effect on threonine phosphorylation of the molecules. The FRD and E2 treatment did not influence Erk 1/2 expression and phosphorylation and heart mass as well. The data show that E2 selectively suppress the negative effects of a FRD on Akt/eNOS signalling and probably point to the different effects of E2 on kinase/phosphatase pathways responsible for phosphorylation/dephosphorylation of Akt and eNOS. Furthermore, the results suggest that the heart of females in the reproductive period is partially protected against the damaging effects of increased fructose intake.",
journal = "British Journal of Nutrition",
title = "Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?",
volume = "109",
number = "11",
pages = "1940-1948",
doi = "10.1017/S0007114512004114"
}
Romić, S. Đ., Tepavčević, S., Žakula, Z., Milosavljević, T., Stojiljković, M. D., Živković, M., Popović, M., Stanković, A.,& Korićanac, G. (2013). Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?.
British Journal of Nutrition, 109(11), 1940-1948.
https://doi.org/10.1017/S0007114512004114
Romić SĐ, Tepavčević S, Žakula Z, Milosavljević T, Stojiljković MD, Živković M, Popović M, Stanković A, Korićanac G. Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?. British Journal of Nutrition. 2013;109(11):1940-1948
Romić Snježana Đ., Tepavčević Snežana, Žakula Zorica, Milosavljević Tijana, Stojiljković Mojca D., Živković Maja, Popović Milan, Stanković Aleksandra, Korićanac Goran, "Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?" British Journal of Nutrition, 109, no. 11 (2013):1940-1948,
https://doi.org/10.1017/S0007114512004114 .
1
10
9
9

The Expression of Ace, Ace2, At1 and At2 Receptors in the Heart of Fructose Fed Ovariectomised Rats-Effect of Estradiol

Bundalo, Maja M.; Tepavčević, Snežana; Romić, Snježana Đ.; Korićanac, Goran; Živković, Maja; Stanković, Aleksandra

(2013)

TY  - CONF
AU  - Bundalo, Maja M.
AU  - Tepavčević, Snežana
AU  - Romić, Snježana Đ.
AU  - Korićanac, Goran
AU  - Živković, Maja
AU  - Stanković, Aleksandra
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5741
C3  - Cardiology
T1  - The Expression of Ace, Ace2, At1 and At2 Receptors in the Heart of Fructose Fed Ovariectomised Rats-Effect of Estradiol
VL  - 126
SP  - 353
EP  - 353
ER  - 
@conference{
author = "Bundalo, Maja M. and Tepavčević, Snežana and Romić, Snježana Đ. and Korićanac, Goran and Živković, Maja and Stanković, Aleksandra",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5741",
journal = "Cardiology",
title = "The Expression of Ace, Ace2, At1 and At2 Receptors in the Heart of Fructose Fed Ovariectomised Rats-Effect of Estradiol",
volume = "126",
pages = "353-353"
}
Bundalo, M. M., Tepavčević, S., Romić, S. Đ., Korićanac, G., Živković, M.,& Stanković, A. (2013). The Expression of Ace, Ace2, At1 and At2 Receptors in the Heart of Fructose Fed Ovariectomised Rats-Effect of Estradiol.
Cardiology, 126, 353-353.
Bundalo MM, Tepavčević S, Romić SĐ, Korićanac G, Živković M, Stanković A. The Expression of Ace, Ace2, At1 and At2 Receptors in the Heart of Fructose Fed Ovariectomised Rats-Effect of Estradiol. Cardiology. 2013;126:353-353
Bundalo Maja M., Tepavčević Snežana, Romić Snježana Đ., Korićanac Goran, Živković Maja, Stanković Aleksandra, "The Expression of Ace, Ace2, At1 and At2 Receptors in the Heart of Fructose Fed Ovariectomised Rats-Effect of Estradiol" Cardiology, 126 (2013):353-353

Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity

Stojiljković, Mojca D.; Žakula, Zorica; Korićanac, Goran; Milosavljević, Tijana; Tepavčević, Snežana; Sudar, Emina; Isenović, Esma R.

(2012)

TY  - JOUR
AU  - Stojiljković, Mojca D.
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Milosavljević, Tijana
AU  - Tepavčević, Snežana
AU  - Sudar, Emina
AU  - Isenović, Esma R.
PY  - 2012
UR  - http://openurl.ingenta.com/content/xref?genre=article&issn=1936-6612&volume=5&issue=2&spage=566
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7801
AB  - The aim of our study was to characterize the acute effects of streptozotocin-induced diabetes on the regulation of cardiac endothelial and inducibile nitric oxide synthase and related signaling pathways. Over the past decade, it has become increasing apparent that competition between the nitric oxide synthase and arginase pathways for L-arginin limits nitric oxid production. Imbalance between these pathways may contribute to heart disfunction especially in diabetes. To evaluate the role of insulin in regulation of endothelial and inducible nitric oxide synthase through phosphatidylinositol 3-kinase/protein kinase B and extracellular signaling-regulated kinase 1 and 2 signaling pathways, male Wistar rats were injected with streptozotocin (65 mg/kg i.p.). Diabetic animals were either maintained untreated for 2 weeks or treated with insulin (3 IU/animal s.c.) for seven days. The arginase activity in diabetic rat heart was augmented, followed by reduction of L-arginine. Insulin treatment significantly decreased arginase activity in heart but it still remained high compare to control rats. Diabetes and insulin treatment did not change endothelial nitric oxide synthase protein and mRNA expression in the heart. In contrast, phosphorylation of endothelial nitric oxide synthase was decreased in diabetic rats and insulin restored it to the control level. Insulin treatment caused increase in inducibile nitric oxide synthase mRNA content. Protein and mRNA expression of cardiac protein kinase B were not altered in diabetic and insulin treated rats, but protein kinase B phosphorylation was lower in diabetes and restored after insulin administration. In addition, insulin deficiency significantly decreases extracellular signaling-regulated kinase 1 and 2 phosphorylation in the heart and insulin treatment partially ameliorates this decline. These data suggest that in the early stage of diabetes arginase is markedly induced in heart and increased arginase activity preceded alterations of inducibile nitric oxide synthase expression/activity. © 2012 American Scientific Publishers All rights reserved.
T2  - Advanced Science Letters
T1  - Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity
VL  - 5
IS  - 2
SP  - 566
EP  - 574
DO  - 10.1166/asl.2012.3254
ER  - 
@article{
author = "Stojiljković, Mojca D. and Žakula, Zorica and Korićanac, Goran and Milosavljević, Tijana and Tepavčević, Snežana and Sudar, Emina and Isenović, Esma R.",
year = "2012",
url = "http://openurl.ingenta.com/content/xref?genre=article&issn=1936-6612&volume=5&issue=2&spage=566, http://vinar.vin.bg.ac.rs/handle/123456789/7801",
abstract = "The aim of our study was to characterize the acute effects of streptozotocin-induced diabetes on the regulation of cardiac endothelial and inducibile nitric oxide synthase and related signaling pathways. Over the past decade, it has become increasing apparent that competition between the nitric oxide synthase and arginase pathways for L-arginin limits nitric oxid production. Imbalance between these pathways may contribute to heart disfunction especially in diabetes. To evaluate the role of insulin in regulation of endothelial and inducible nitric oxide synthase through phosphatidylinositol 3-kinase/protein kinase B and extracellular signaling-regulated kinase 1 and 2 signaling pathways, male Wistar rats were injected with streptozotocin (65 mg/kg i.p.). Diabetic animals were either maintained untreated for 2 weeks or treated with insulin (3 IU/animal s.c.) for seven days. The arginase activity in diabetic rat heart was augmented, followed by reduction of L-arginine. Insulin treatment significantly decreased arginase activity in heart but it still remained high compare to control rats. Diabetes and insulin treatment did not change endothelial nitric oxide synthase protein and mRNA expression in the heart. In contrast, phosphorylation of endothelial nitric oxide synthase was decreased in diabetic rats and insulin restored it to the control level. Insulin treatment caused increase in inducibile nitric oxide synthase mRNA content. Protein and mRNA expression of cardiac protein kinase B were not altered in diabetic and insulin treated rats, but protein kinase B phosphorylation was lower in diabetes and restored after insulin administration. In addition, insulin deficiency significantly decreases extracellular signaling-regulated kinase 1 and 2 phosphorylation in the heart and insulin treatment partially ameliorates this decline. These data suggest that in the early stage of diabetes arginase is markedly induced in heart and increased arginase activity preceded alterations of inducibile nitric oxide synthase expression/activity. © 2012 American Scientific Publishers All rights reserved.",
journal = "Advanced Science Letters",
title = "Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity",
volume = "5",
number = "2",
pages = "566-574",
doi = "10.1166/asl.2012.3254"
}
Stojiljković, M. D., Žakula, Z., Korićanac, G., Milosavljević, T., Tepavčević, S., Sudar, E.,& Isenović, E. R. (2012). Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity.
Advanced Science Letters, 5(2), 566-574.
https://doi.org/10.1166/asl.2012.3254
Stojiljković MD, Žakula Z, Korićanac G, Milosavljević T, Tepavčević S, Sudar E, Isenović ER. Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity. Advanced Science Letters. 2012;5(2):566-574
Stojiljković Mojca D., Žakula Zorica, Korićanac Goran, Milosavljević Tijana, Tepavčević Snežana, Sudar Emina, Isenović Esma R., "Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity" Advanced Science Letters, 5, no. 2 (2012):566-574,
https://doi.org/10.1166/asl.2012.3254 .
1

Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation

Korićanac, Goran; Tepavčević, Snežana; Romić, Snježana Đ.; Živković, Maja; Stojiljković, Mojca D.; Milosavljević, Tijana; Stanković, Aleksandra; Petković, Marijana; Kamceva, Tina; Žakula, Zorica

(2012)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Romić, Snježana Đ.
AU  - Živković, Maja
AU  - Stojiljković, Mojca D.
AU  - Milosavljević, Tijana
AU  - Stanković, Aleksandra
AU  - Petković, Marijana
AU  - Kamceva, Tina
AU  - Žakula, Zorica
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5104
AB  - Fructose rich diet increases hepatic triglycerides production and has deleterious cardiac effects. Estrogens are involved in regulation of lipid metabolism as well, but their effects are cardio beneficial. In order to study effects of fructose rich diet on the main heart fatty acid transporter CD36 and the role of estrogens, we subjected ovariectomized female rats to the standard diet or fructose rich diet, with or without estradiol (E2) replacement. The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. Results show that fructose rich diet significantly increased plasma triglycerides and decreased plasma free fatty acid (FFA) concentration, while E2 additionally emphasized FFA decrease. The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsomes content. The E2 in fructose-fed rats raised the total cardiac protein content of CD36, its presence in plasma membranes and low density microsomes, and cardiac deposition of triglycerides, as well. Although E2 counteracts fructose in some aspects of lipid metabolism, and separately they have opposite cardiac effects, in combination with fructose rich diet, E2 additionally enhances CD36 presence in plasma membranes of cardiac cells and triglycerides accumulation, which paradoxically might promote deleterious effects of fructose diet on cardiac lipid metabolism. Taken together, the results presented in this work are of high importance for clinical administration of estrogens in females with a history of type 2 diabetes. (C) 2012 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation
VL  - 694
IS  - 1-3
SP  - 127
EP  - 134
DO  - 10.1016/j.ejphar.2012.08.007
ER  - 
@article{
author = "Korićanac, Goran and Tepavčević, Snežana and Romić, Snježana Đ. and Živković, Maja and Stojiljković, Mojca D. and Milosavljević, Tijana and Stanković, Aleksandra and Petković, Marijana and Kamceva, Tina and Žakula, Zorica",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5104",
abstract = "Fructose rich diet increases hepatic triglycerides production and has deleterious cardiac effects. Estrogens are involved in regulation of lipid metabolism as well, but their effects are cardio beneficial. In order to study effects of fructose rich diet on the main heart fatty acid transporter CD36 and the role of estrogens, we subjected ovariectomized female rats to the standard diet or fructose rich diet, with or without estradiol (E2) replacement. The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. Results show that fructose rich diet significantly increased plasma triglycerides and decreased plasma free fatty acid (FFA) concentration, while E2 additionally emphasized FFA decrease. The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsomes content. The E2 in fructose-fed rats raised the total cardiac protein content of CD36, its presence in plasma membranes and low density microsomes, and cardiac deposition of triglycerides, as well. Although E2 counteracts fructose in some aspects of lipid metabolism, and separately they have opposite cardiac effects, in combination with fructose rich diet, E2 additionally enhances CD36 presence in plasma membranes of cardiac cells and triglycerides accumulation, which paradoxically might promote deleterious effects of fructose diet on cardiac lipid metabolism. Taken together, the results presented in this work are of high importance for clinical administration of estrogens in females with a history of type 2 diabetes. (C) 2012 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation",
volume = "694",
number = "1-3",
pages = "127-134",
doi = "10.1016/j.ejphar.2012.08.007"
}
Korićanac, G., Tepavčević, S., Romić, S. Đ., Živković, M., Stojiljković, M. D., Milosavljević, T., Stanković, A., Petković, M., Kamceva, T.,& Žakula, Z. (2012). Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation.
European Journal of Pharmacology, 694(1-3), 127-134.
https://doi.org/10.1016/j.ejphar.2012.08.007
Korićanac G, Tepavčević S, Romić SĐ, Živković M, Stojiljković MD, Milosavljević T, Stanković A, Petković M, Kamceva T, Žakula Z. Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation. European Journal of Pharmacology. 2012;694(1-3):127-134
Korićanac Goran, Tepavčević Snežana, Romić Snježana Đ., Živković Maja, Stojiljković Mojca D., Milosavljević Tijana, Stanković Aleksandra, Petković Marijana, Kamceva Tina, Žakula Zorica, "Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation" European Journal of Pharmacology, 694, no. 1-3 (2012):127-134,
https://doi.org/10.1016/j.ejphar.2012.08.007 .
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Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase

Korićanac, Goran; Tepavčević, Snežana; Žakula, Zorica; Milosavljević, Tijana; Stojiljković, Mojca D.; Isenović, Esma R.

(2011)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Žakula, Zorica
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Isenović, Esma R.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4254
AB  - Insulin and estradiol share some of signaling pathways and regulate same target molecules exerting mostly beneficial cardiac effects. in order to study their cardiac interaction, ovariectomized female rats were treated with hormones, separately or simultaneously (20,30 or 40 min before analysis), and the phosphorylations of protein kinase B (Akt), extracellular signal-regulated kinases 1 and 2 (ERK 1/2), endothelial nitric oxide synthase (eNOS) were analyzed, as well as the plasma membrane content of alpha 2 subunit of Na+/K+-ATPase. Insulin, particularly, and estradiol stimulate Ser(473) Akt phosphorylation. The combined treatment was stimulatory, but less than insulin alone was. The general increase of Thr(308) Akt phosphorylation by insulin was stronger than at Ser(473) and reduced in the presence of estradiol, which also stimulated this phosphorylation given alone. The estradiol induction of ERK 1/2 phosphorylation was inverted to the decrease by the combined treatment, while insulin had no effect. Only insulin increased the plasma membrane content of alpha 2. Estradiol did increase the phosphorylation of eNOS, whereas the insulin effect was controversial. The effect of the combined treatment on target molecules was generally opposite to single hormone treatment. In summary, both hormones exerted an effect on Akt phosphorylation, but only estradiol stimulated ERK 1/2 phosphorylation. The alpha 2 plasma membrane content was increased only by insulin, while estradiol increased eNOS phosphorylation more consistently. Finally, if these hormones were administered together, it seems that they disturb each other in having a full effect on cardiac Akt, ERK 1/2, and downstream effectors, eNOS and Na+/K+-ATPase. (c) 2011 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase
VL  - 655
IS  - 1-3
SP  - 23
EP  - 30
DO  - 10.1016/j.ejphar.2011.01.016
ER  - 
@article{
author = "Korićanac, Goran and Tepavčević, Snežana and Žakula, Zorica and Milosavljević, Tijana and Stojiljković, Mojca D. and Isenović, Esma R.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4254",
abstract = "Insulin and estradiol share some of signaling pathways and regulate same target molecules exerting mostly beneficial cardiac effects. in order to study their cardiac interaction, ovariectomized female rats were treated with hormones, separately or simultaneously (20,30 or 40 min before analysis), and the phosphorylations of protein kinase B (Akt), extracellular signal-regulated kinases 1 and 2 (ERK 1/2), endothelial nitric oxide synthase (eNOS) were analyzed, as well as the plasma membrane content of alpha 2 subunit of Na+/K+-ATPase. Insulin, particularly, and estradiol stimulate Ser(473) Akt phosphorylation. The combined treatment was stimulatory, but less than insulin alone was. The general increase of Thr(308) Akt phosphorylation by insulin was stronger than at Ser(473) and reduced in the presence of estradiol, which also stimulated this phosphorylation given alone. The estradiol induction of ERK 1/2 phosphorylation was inverted to the decrease by the combined treatment, while insulin had no effect. Only insulin increased the plasma membrane content of alpha 2. Estradiol did increase the phosphorylation of eNOS, whereas the insulin effect was controversial. The effect of the combined treatment on target molecules was generally opposite to single hormone treatment. In summary, both hormones exerted an effect on Akt phosphorylation, but only estradiol stimulated ERK 1/2 phosphorylation. The alpha 2 plasma membrane content was increased only by insulin, while estradiol increased eNOS phosphorylation more consistently. Finally, if these hormones were administered together, it seems that they disturb each other in having a full effect on cardiac Akt, ERK 1/2, and downstream effectors, eNOS and Na+/K+-ATPase. (c) 2011 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase",
volume = "655",
number = "1-3",
pages = "23-30",
doi = "10.1016/j.ejphar.2011.01.016"
}
Korićanac, G., Tepavčević, S., Žakula, Z., Milosavljević, T., Stojiljković, M. D.,& Isenović, E. R. (2011). Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase.
European Journal of Pharmacology, 655(1-3), 23-30.
https://doi.org/10.1016/j.ejphar.2011.01.016
Korićanac G, Tepavčević S, Žakula Z, Milosavljević T, Stojiljković MD, Isenović ER. Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase. European Journal of Pharmacology. 2011;655(1-3):23-30
Korićanac Goran, Tepavčević Snežana, Žakula Zorica, Milosavljević Tijana, Stojiljković Mojca D., Isenović Esma R., "Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase" European Journal of Pharmacology, 655, no. 1-3 (2011):23-30,
https://doi.org/10.1016/j.ejphar.2011.01.016 .
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