Stojiljković, Mojca D.

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Authority KeyName Variants
orcid::0000-0002-9041-7947
  • Stojiljković, Mojca D. (22)
  • Vulović, Mojica (8)
Projects

Author's Bibliography

Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2

Stanišić, Jelena; Ivković, Tamara; Romić, Snježana Đ.; Zec, Manja; Ćulafić, Tijana; Stojiljković, Mojca D.; Korićanac, Goran

(2021)

TY  - JOUR
AU  - Stanišić, Jelena
AU  - Ivković, Tamara
AU  - Romić, Snježana Đ.
AU  - Zec, Manja
AU  - Ćulafić, Tijana
AU  - Stojiljković, Mojca D.
AU  - Korićanac, Goran
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9110
AB  - Consumption of walnuts is beneficial for cardiovascular health. To study walnut effects on proteins involved in vascular tone regulation, control and fructose-fed rats were subjected to walnut diet for 6 weeks. In contrast with increased energy intake and body mass gain, aortic protein level of L-type calcium channel alpha subunit was decreased and the level of SUR2B subunit of ATP-sensitive K + channel was increased in healthy rats subjected to walnuts, together with improved Akt phosphorylation. Upon the walnut diet in rats subjected to fructose overload, the rise in energy intake and body mass gain, was followed by an increase in blood insulin. Although SUR2B level was elevated, the level of sodium-calcium exchanger NCX1 and inducible nitric oxide synthase were reduced and increased, respectively. In summary, walnut consumption was accompanied with moderate beneficial vascular effect in healthy rats, while an effect of walnut in rats with metabolic disturbances was rather controversial.
T2  - International Journal of Food Sciences and Nutrition
T1  - Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2
VL  - 72
IS  - 3
SP  - 324
EP  - 334
DO  - 10.1080/09637486.2020.1796931
ER  - 
@article{
author = "Stanišić, Jelena and Ivković, Tamara and Romić, Snježana Đ. and Zec, Manja and Ćulafić, Tijana and Stojiljković, Mojca D. and Korićanac, Goran",
year = "2021",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/9110",
abstract = "Consumption of walnuts is beneficial for cardiovascular health. To study walnut effects on proteins involved in vascular tone regulation, control and fructose-fed rats were subjected to walnut diet for 6 weeks. In contrast with increased energy intake and body mass gain, aortic protein level of L-type calcium channel alpha subunit was decreased and the level of SUR2B subunit of ATP-sensitive K + channel was increased in healthy rats subjected to walnuts, together with improved Akt phosphorylation. Upon the walnut diet in rats subjected to fructose overload, the rise in energy intake and body mass gain, was followed by an increase in blood insulin. Although SUR2B level was elevated, the level of sodium-calcium exchanger NCX1 and inducible nitric oxide synthase were reduced and increased, respectively. In summary, walnut consumption was accompanied with moderate beneficial vascular effect in healthy rats, while an effect of walnut in rats with metabolic disturbances was rather controversial.",
journal = "International Journal of Food Sciences and Nutrition",
title = "Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2",
volume = "72",
number = "3",
pages = "324-334",
doi = "10.1080/09637486.2020.1796931"
}
Stanišić, J., Ivković, T., Romić, S. Đ., Zec, M., Ćulafić, T., Stojiljković, M. D.,& Korićanac, G. (2021). Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2.
International Journal of Food Sciences and Nutrition, 72(3), 324-334.
https://doi.org/10.1080/09637486.2020.1796931
Stanišić J, Ivković T, Romić SĐ, Zec M, Ćulafić T, Stojiljković MD, Korićanac G. Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2. International Journal of Food Sciences and Nutrition. 2021;72(3):324-334
Stanišić Jelena, Ivković Tamara, Romić Snježana Đ., Zec Manja, Ćulafić Tijana, Stojiljković Mojca D., Korićanac Goran, "Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2" International Journal of Food Sciences and Nutrition, 72, no. 3 (2021):324-334,
https://doi.org/10.1080/09637486.2020.1796931 .
3
2
1

Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2

Stanišić, Jelena; Ivković, Tamara; Romić, Snježana Đ.; Zec, Manja; Ćulafić, Tijana; Stojiljković, Mojca D.; Korićanac, Goran

(2021)

TY  - JOUR
AU  - Stanišić, Jelena
AU  - Ivković, Tamara
AU  - Romić, Snježana Đ.
AU  - Zec, Manja
AU  - Ćulafić, Tijana
AU  - Stojiljković, Mojca D.
AU  - Korićanac, Goran
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9103
AB  - Consumption of walnuts is beneficial for cardiovascular health. To study walnut effects on proteins involved in vascular tone regulation, control and fructose-fed rats were subjected to walnut diet for 6 weeks. In contrast with increased energy intake and body mass gain, aortic protein level of L-type calcium channel alpha subunit was decreased and the level of SUR2B subunit of ATP-sensitive K + channel was increased in healthy rats subjected to walnuts, together with improved Akt phosphorylation. Upon the walnut diet in rats subjected to fructose overload, the rise in energy intake and body mass gain, was followed by an increase in blood insulin. Although SUR2B level was elevated, the level of sodium-calcium exchanger NCX1 and inducible nitric oxide synthase were reduced and increased, respectively. In summary, walnut consumption was accompanied with moderate beneficial vascular effect in healthy rats, while an effect of walnut in rats with metabolic disturbances was rather controversial.
T2  - International Journal of Food Sciences and Nutrition
T1  - Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2
VL  - 72
IS  - 3
SP  - 324
EP  - 334
DO  - 10.1080/09637486.2020.1796931
ER  - 
@article{
author = "Stanišić, Jelena and Ivković, Tamara and Romić, Snježana Đ. and Zec, Manja and Ćulafić, Tijana and Stojiljković, Mojca D. and Korićanac, Goran",
year = "2021",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/9103",
abstract = "Consumption of walnuts is beneficial for cardiovascular health. To study walnut effects on proteins involved in vascular tone regulation, control and fructose-fed rats were subjected to walnut diet for 6 weeks. In contrast with increased energy intake and body mass gain, aortic protein level of L-type calcium channel alpha subunit was decreased and the level of SUR2B subunit of ATP-sensitive K + channel was increased in healthy rats subjected to walnuts, together with improved Akt phosphorylation. Upon the walnut diet in rats subjected to fructose overload, the rise in energy intake and body mass gain, was followed by an increase in blood insulin. Although SUR2B level was elevated, the level of sodium-calcium exchanger NCX1 and inducible nitric oxide synthase were reduced and increased, respectively. In summary, walnut consumption was accompanied with moderate beneficial vascular effect in healthy rats, while an effect of walnut in rats with metabolic disturbances was rather controversial.",
journal = "International Journal of Food Sciences and Nutrition",
title = "Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2",
volume = "72",
number = "3",
pages = "324-334",
doi = "10.1080/09637486.2020.1796931"
}
Stanišić, J., Ivković, T., Romić, S. Đ., Zec, M., Ćulafić, T., Stojiljković, M. D.,& Korićanac, G. (2021). Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2.
International Journal of Food Sciences and Nutrition, 72(3), 324-334.
https://doi.org/10.1080/09637486.2020.1796931
Stanišić J, Ivković T, Romić SĐ, Zec M, Ćulafić T, Stojiljković MD, Korićanac G. Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2. International Journal of Food Sciences and Nutrition. 2021;72(3):324-334
Stanišić Jelena, Ivković Tamara, Romić Snježana Đ., Zec Manja, Ćulafić Tijana, Stojiljković Mojca D., Korićanac Goran, "Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2" International Journal of Food Sciences and Nutrition, 72, no. 3 (2021):324-334,
https://doi.org/10.1080/09637486.2020.1796931 .
3
2
1

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

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 .

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

Estradiol Protects Ovariectomized Female Rats Against Fructose-Rich Diet Induced Oxidative Stress

Bošković, Maja; Bundalo, Maja M.; Stojiljković, Mojca D.; Kostić, Milan; Živković, Maja; Korićanac, Goran; Stanković, Aleksandra; Životić, Ivan

(2017)

TY  - CONF
AU  - Bošković, Maja
AU  - Bundalo, Maja M.
AU  - Stojiljković, Mojca D.
AU  - Kostić, Milan
AU  - Živković, Maja
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
AU  - Životić, Ivan
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7179
C3  - Atherosclerosis
T1  - Estradiol Protects Ovariectomized Female Rats Against Fructose-Rich Diet Induced Oxidative Stress
VL  - 263
SP  - E192
EP  - E192
DO  - 10.1016/j.atherosclerosis.2017.06.616
ER  - 
@conference{
author = "Bošković, Maja and Bundalo, Maja M. and Stojiljković, Mojca D. and Kostić, Milan and Živković, Maja and Korićanac, Goran and Stanković, Aleksandra and Životić, Ivan",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/7179",
journal = "Atherosclerosis",
title = "Estradiol Protects Ovariectomized Female Rats Against Fructose-Rich Diet Induced Oxidative Stress",
volume = "263",
pages = "E192-E192",
doi = "10.1016/j.atherosclerosis.2017.06.616"
}
Bošković, M., Bundalo, M. M., Stojiljković, M. D., Kostić, M., Živković, M., Korićanac, G., Stanković, A.,& Životić, I. (2017). Estradiol Protects Ovariectomized Female Rats Against Fructose-Rich Diet Induced Oxidative Stress.
Atherosclerosis, 263, E192-E192.
https://doi.org/10.1016/j.atherosclerosis.2017.06.616
Bošković M, Bundalo MM, Stojiljković MD, Kostić M, Živković M, Korićanac G, Stanković A, Životić I. Estradiol Protects Ovariectomized Female Rats Against Fructose-Rich Diet Induced Oxidative Stress. Atherosclerosis. 2017;263:E192-E192
Bošković Maja, Bundalo Maja M., Stojiljković Mojca D., Kostić Milan, Živković Maja, Korićanac Goran, Stanković Aleksandra, Životić Ivan, "Estradiol Protects Ovariectomized Female Rats Against Fructose-Rich Diet Induced Oxidative Stress" Atherosclerosis, 263 (2017):E192-E192,
https://doi.org/10.1016/j.atherosclerosis.2017.06.616 .

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
14
11

Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation

Bundalo, Maja M.; Živković, Maja; Ćulafić, Tijana; Stojiljković, Mojca D.; Korićanac, Goran; Stanković, Aleksandra

(2015)

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Živković, Maja
AU  - Ćulafić, Tijana
AU  - Stojiljković, Mojca D.
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1112
AB  - Fructose-rich diet induces metabolic changes similar to those observed in metabolic syndrome. Among other matrix metalloproteinases, MMP-9 has an important role in adverse cardiac remodelling and might have a role in the development of cardiovascular disorders associated with metabolic syndrome. The changes of MMP-9 expression could be mediated via the NF kappa B pathway. In this study we investigated the effect of fructose-rich diet on MMP-9 expression in the heart of male and female rats, along with the effect of fructose-rich diet and oestradiol on MMP-9 expression in ovariectomized females. We further assessed the effect of fructose-rich diet and oestradiol on NF kappa B activation, measured as the level of p65 phosphorylation at Ser 276. The results showed that the diet regime did not affect the heart mass. Higher MMP-9 gene expression was found in cardiac tissue of male rats fed the fructose-rich diet than in females on the same diet regime. In ovariectomized females, fructose-rich diet upregulated MMP-9 protein and mRNA expression in the heart, as well as phosphorylation of the p65 subunit of NF kappa B at Ser 276. Oestradiol replacement therapy reverted these changes in the heart of ovariectomized females. This study has shown that oestradiol could revert the early molecular changes in MMP-9 expression induced by fructose-rich diet that occurred before cardiac hypertrophy development by decreasing phosphorylation of the NF kappa B p65 subunit at Ser 276.
T2  - Folia Biologica
T1  - Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation
VL  - 61
IS  - 6
SP  - 233
EP  - 240
ER  - 
@article{
author = "Bundalo, Maja M. and Živković, Maja and Ćulafić, Tijana and Stojiljković, Mojca D. and Korićanac, Goran and Stanković, Aleksandra",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1112",
abstract = "Fructose-rich diet induces metabolic changes similar to those observed in metabolic syndrome. Among other matrix metalloproteinases, MMP-9 has an important role in adverse cardiac remodelling and might have a role in the development of cardiovascular disorders associated with metabolic syndrome. The changes of MMP-9 expression could be mediated via the NF kappa B pathway. In this study we investigated the effect of fructose-rich diet on MMP-9 expression in the heart of male and female rats, along with the effect of fructose-rich diet and oestradiol on MMP-9 expression in ovariectomized females. We further assessed the effect of fructose-rich diet and oestradiol on NF kappa B activation, measured as the level of p65 phosphorylation at Ser 276. The results showed that the diet regime did not affect the heart mass. Higher MMP-9 gene expression was found in cardiac tissue of male rats fed the fructose-rich diet than in females on the same diet regime. In ovariectomized females, fructose-rich diet upregulated MMP-9 protein and mRNA expression in the heart, as well as phosphorylation of the p65 subunit of NF kappa B at Ser 276. Oestradiol replacement therapy reverted these changes in the heart of ovariectomized females. This study has shown that oestradiol could revert the early molecular changes in MMP-9 expression induced by fructose-rich diet that occurred before cardiac hypertrophy development by decreasing phosphorylation of the NF kappa B p65 subunit at Ser 276.",
journal = "Folia Biologica",
title = "Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation",
volume = "61",
number = "6",
pages = "233-240"
}
Bundalo, M. M., Živković, M., Ćulafić, T., Stojiljković, M. D., Korićanac, G.,& Stanković, A. (2015). Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation.
Folia Biologica, 61(6), 233-240.
Bundalo MM, Živković M, Ćulafić T, Stojiljković MD, Korićanac G, Stanković A. Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation. Folia Biologica. 2015;61(6):233-240
Bundalo Maja M., Živković Maja, Ćulafić Tijana, Stojiljković Mojca D., Korićanac Goran, Stanković Aleksandra, "Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation" Folia Biologica, 61, no. 6 (2015):233-240
7
6

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

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

Efekat eksperimentalnog dijabetesa tipa 1 i supstitucione terapije na molekule regulisane insulinom u srcu pacova

Stojiljković, Mojca D.

(Универзитет у Београду, Биолошки факултет, 2014)

TY  - BOOK
AU  - Stojiljković, Mojca D.
PY  - 2014
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=3811
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:12801/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1024763058
UR  - http://nardus.mpn.gov.rs/123456789/6495
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7302
AB  - Insulinska deficijencija i hiperglikemija, koje predstavljaju osnovnekarakteristike dijabetesa tipa 1, povezane su sa brojnim endokrinim imetaboličkim promenama, a jedna od najčešćih komplikacija je povećanaučestalost nastanka kardiovaskularnih oboljenja. Zbog toga je rana i adekvatnaprimena terapije insulinom neophodna, kako za kontrolu bolesti, tako i zaprevenciju potencijalnih komplikacija.Polazna hipoteza istraţivanja čiji su rezultati obuhvaćeni ovomdoktorskom disertacijom je bila da u stanju hipoinsulinemije i hiperglikemijemoţe doći do promena u signalnom putu insulina u srcu, što moţe da se odrazina produkciju azot-monoksida i iskorišćavanje energetskih supstrata, a da bisupstitucija insulinom trebala da koriguje nastale promene.Za uspostavljanje eksperimentalnog modela dijabetesa tipa 1, muţjacipacova soja Wistar tretirani su streptozotocinom (60 mg/kg). Poznato je da seakutni dijabetes javlja između osmog dana i tri nedelje, a hronični 3 nedeljenakon tretmana streptozotocinom. Ţivotinje sa dijabetesom su ili bilenetretirane 2 nedelje ili podvrgnute subhroničnom tretmanu insulinom (3 IU) utrajanju od 7 dana. Za analizu su selektirani signalni molekuli Akt i ERK kojipredstavljaju medijatore gotovo svih efekata insulina u srcu. Osim togaanalizirani su i efektorni molekuli regulisani preko aktivacije signalnih putevaAkt i ERK, kao što su eNOS i iNOS, uključeni u sintezu azot-monoksida, kao itransporteri glukoze GLUT1 i GLUT4 i transporter masnih kiselina CD36.Ispitivana je ekspresija ovih molekula na nivou gena i proteina i/ili fosforilacija,kao i unutarćelijska lokalizacija transportera za glukozu i masne kiseline u srcu.Poznato je da je kompeticija između arginaze i NOS za zajedničkisupstrat L-arginin, ograničavajući faktor za proizvodnju azot-monoksida...
AB  - nsulin deficiency and hyperglycemia, which are the main features ofType 1 diabetes are associated with a number of endocrine and metabolicdisorders and one of the most common complications is the increased incidenceof cardiovascular diseases. Therefore, appropriate insulin replacement therapyis necessary in order to control the disease, as well as for the prevention ofpotential complications.We hypothesized that insulin deficiency and hyperglycemia may lead tochanges in cardiac insulin signalling pathway which consequently may result inchanges in nitric oxide production and utilization of energy substrates, and thatinsulin replacement is required to correct the changes.To induce experimental Type 1 diabetes, male Wistar rats were injectedintraperitoneally with streptozotocin (65 mg/kg). Acute diabetes was reportedto occur between 8 days and 3 weeks, and chronic diabetes within 3 weeks afterstreptozotocin administration. Diabetic animals were either maintaineduntreated, or treated with insulin (3 IU) daily for a week. For analysis,intracellular signaling molecules Akt and ERK1/2 were selected, which areimportant intermediary of almost all effects of insulin in the heart. Furthermorewe analyzed effector molecules which are regulated through activation of Aktand ERK signaling pathways, such as eNOS and iNOS, involved in thesynthesis of nitric oxide, as well as glucose transporter GLUT1 and GLUT4 andtransporter of fatty acids CD36. In the present study we examined theexpression and/or phosphorylation of the molecules, as well as the subcellularlocalization of the transporters for glucose and fatty acid in the heart.It is known that the competition between arginase and NOS for acommon substrate L-arginine is a limiting factor for the production of nitricoxide...
PB  - Универзитет у Београду, Биолошки факултет
T2  - Универзитет у Београду
T1  - Efekat eksperimentalnog dijabetesa tipa 1 i supstitucione terapije na molekule regulisane insulinom u srcu pacova
T1  - The effect of experimentally induced Type 1 diabetes and insulin replacement therapy on insulin signalling pathways in the rat heart
ER  - 
@phdthesis{
author = "Stojiljković, Mojca D.",
year = "2014",
url = "http://eteze.bg.ac.rs/application/showtheses?thesesId=3811, https://fedorabg.bg.ac.rs/fedora/get/o:12801/bdef:Content/download, http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1024763058, http://nardus.mpn.gov.rs/123456789/6495, http://vinar.vin.bg.ac.rs/handle/123456789/7302",
abstract = "Insulinska deficijencija i hiperglikemija, koje predstavljaju osnovnekarakteristike dijabetesa tipa 1, povezane su sa brojnim endokrinim imetaboličkim promenama, a jedna od najčešćih komplikacija je povećanaučestalost nastanka kardiovaskularnih oboljenja. Zbog toga je rana i adekvatnaprimena terapije insulinom neophodna, kako za kontrolu bolesti, tako i zaprevenciju potencijalnih komplikacija.Polazna hipoteza istraţivanja čiji su rezultati obuhvaćeni ovomdoktorskom disertacijom je bila da u stanju hipoinsulinemije i hiperglikemijemoţe doći do promena u signalnom putu insulina u srcu, što moţe da se odrazina produkciju azot-monoksida i iskorišćavanje energetskih supstrata, a da bisupstitucija insulinom trebala da koriguje nastale promene.Za uspostavljanje eksperimentalnog modela dijabetesa tipa 1, muţjacipacova soja Wistar tretirani su streptozotocinom (60 mg/kg). Poznato je da seakutni dijabetes javlja između osmog dana i tri nedelje, a hronični 3 nedeljenakon tretmana streptozotocinom. Ţivotinje sa dijabetesom su ili bilenetretirane 2 nedelje ili podvrgnute subhroničnom tretmanu insulinom (3 IU) utrajanju od 7 dana. Za analizu su selektirani signalni molekuli Akt i ERK kojipredstavljaju medijatore gotovo svih efekata insulina u srcu. Osim togaanalizirani su i efektorni molekuli regulisani preko aktivacije signalnih putevaAkt i ERK, kao što su eNOS i iNOS, uključeni u sintezu azot-monoksida, kao itransporteri glukoze GLUT1 i GLUT4 i transporter masnih kiselina CD36.Ispitivana je ekspresija ovih molekula na nivou gena i proteina i/ili fosforilacija,kao i unutarćelijska lokalizacija transportera za glukozu i masne kiseline u srcu.Poznato je da je kompeticija između arginaze i NOS za zajedničkisupstrat L-arginin, ograničavajući faktor za proizvodnju azot-monoksida..., nsulin deficiency and hyperglycemia, which are the main features ofType 1 diabetes are associated with a number of endocrine and metabolicdisorders and one of the most common complications is the increased incidenceof cardiovascular diseases. Therefore, appropriate insulin replacement therapyis necessary in order to control the disease, as well as for the prevention ofpotential complications.We hypothesized that insulin deficiency and hyperglycemia may lead tochanges in cardiac insulin signalling pathway which consequently may result inchanges in nitric oxide production and utilization of energy substrates, and thatinsulin replacement is required to correct the changes.To induce experimental Type 1 diabetes, male Wistar rats were injectedintraperitoneally with streptozotocin (65 mg/kg). Acute diabetes was reportedto occur between 8 days and 3 weeks, and chronic diabetes within 3 weeks afterstreptozotocin administration. Diabetic animals were either maintaineduntreated, or treated with insulin (3 IU) daily for a week. For analysis,intracellular signaling molecules Akt and ERK1/2 were selected, which areimportant intermediary of almost all effects of insulin in the heart. Furthermorewe analyzed effector molecules which are regulated through activation of Aktand ERK signaling pathways, such as eNOS and iNOS, involved in thesynthesis of nitric oxide, as well as glucose transporter GLUT1 and GLUT4 andtransporter of fatty acids CD36. In the present study we examined theexpression and/or phosphorylation of the molecules, as well as the subcellularlocalization of the transporters for glucose and fatty acid in the heart.It is known that the competition between arginase and NOS for acommon substrate L-arginine is a limiting factor for the production of nitricoxide...",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Efekat eksperimentalnog dijabetesa tipa 1 i supstitucione terapije na molekule regulisane insulinom u srcu pacova, The effect of experimentally induced Type 1 diabetes and insulin replacement therapy on insulin signalling pathways in the rat heart"
}
Stojiljković, M. D. (2014). The effect of experimentally induced Type 1 diabetes and insulin replacement therapy on insulin signalling pathways in the rat heart.
Универзитет у Београду
Универзитет у Београду, Биолошки факултет..
Stojiljković MD. The effect of experimentally induced Type 1 diabetes and insulin replacement therapy on insulin signalling pathways in the rat heart. Универзитет у Београду. 2014;
Stojiljković Mojca D., "The effect of experimentally induced Type 1 diabetes and insulin replacement therapy on insulin signalling pathways in the rat heart" Универзитет у Београду (2014)

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

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 .
14
15
15

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 .
15
15
18

Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters

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

(2011)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Korićanac, Goran
AU  - Žakula, Zorica
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Isenović, Esma R.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4418
AB  - The estrogen binding to specific extranuclear receptors (ER) activates several intracellular pathways that are activated by insulin as well. Moreover, insulin and estradiol (E2) influence cardiac energy substrates, blood glucose and free fatty acids (FFAs), and both hormones exert cardio-beneficial effects. In view of these facts, we suggest that cross-talk between their signaling pathways might have an important role in regulation of cardiac energy substrate transport. Ovariectomized rats were treated with insulin, estradiol (E2), or their combination 20, 30, or 40 min before analysis of blood glucose and FFA level, as well as cardiac plasma membranes (PM) and low density microsomes (LDM) content of glucose (GLUT4 and GLUT1) and FFA (CD36) transporters. Insulin, given alone, or in combination with E2, decreased plasma glucose level at all time points, but did not influence FFA level, while E2 treatment itself did not change glucose and FFA concentration. Insulin increased PM GLUT4 and GLUT1 content 30 and 40 min after treatment and the increases were partially accompanied by decrease in transporter LDM content. E2 increased PM content and decreased LDM content only of GLUT4 at 30 min. Insulin generally, and E2 at 20 min increased CD36 content in PM fraction. Both hormones decreased CD36 LDM content 20 min after administration. Effect of combined treatment mostly did not differ from single hormone treatment, but occasionally, particularly in distribution of GLUT4, combined treatment emphasized single hormone effect, suggesting that insulin and E2 act synergistically in regulation of energy substrate transporters in cardiac tissue.
T2  - Hormone and Metabolic Research
T1  - Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters
VL  - 43
IS  - 8
SP  - 524
EP  - 530
DO  - 10.1055/s-0031-1280784
ER  - 
@article{
author = "Tepavčević, Snežana and Korićanac, Goran and Žakula, Zorica and Milosavljević, Tijana and Stojiljković, Mojca D. and Isenović, Esma R.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4418",
abstract = "The estrogen binding to specific extranuclear receptors (ER) activates several intracellular pathways that are activated by insulin as well. Moreover, insulin and estradiol (E2) influence cardiac energy substrates, blood glucose and free fatty acids (FFAs), and both hormones exert cardio-beneficial effects. In view of these facts, we suggest that cross-talk between their signaling pathways might have an important role in regulation of cardiac energy substrate transport. Ovariectomized rats were treated with insulin, estradiol (E2), or their combination 20, 30, or 40 min before analysis of blood glucose and FFA level, as well as cardiac plasma membranes (PM) and low density microsomes (LDM) content of glucose (GLUT4 and GLUT1) and FFA (CD36) transporters. Insulin, given alone, or in combination with E2, decreased plasma glucose level at all time points, but did not influence FFA level, while E2 treatment itself did not change glucose and FFA concentration. Insulin increased PM GLUT4 and GLUT1 content 30 and 40 min after treatment and the increases were partially accompanied by decrease in transporter LDM content. E2 increased PM content and decreased LDM content only of GLUT4 at 30 min. Insulin generally, and E2 at 20 min increased CD36 content in PM fraction. Both hormones decreased CD36 LDM content 20 min after administration. Effect of combined treatment mostly did not differ from single hormone treatment, but occasionally, particularly in distribution of GLUT4, combined treatment emphasized single hormone effect, suggesting that insulin and E2 act synergistically in regulation of energy substrate transporters in cardiac tissue.",
journal = "Hormone and Metabolic Research",
title = "Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters",
volume = "43",
number = "8",
pages = "524-530",
doi = "10.1055/s-0031-1280784"
}
Tepavčević, S., Korićanac, G., Žakula, Z., Milosavljević, T., Stojiljković, M. D.,& Isenović, E. R. (2011). Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters.
Hormone and Metabolic Research, 43(8), 524-530.
https://doi.org/10.1055/s-0031-1280784
Tepavčević S, Korićanac G, Žakula Z, Milosavljević T, Stojiljković MD, Isenović ER. Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters. Hormone and Metabolic Research. 2011;43(8):524-530
Tepavčević Snežana, Korićanac Goran, Žakula Zorica, Milosavljević Tijana, Stojiljković Mojca D., Isenović Esma R., "Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters" Hormone and Metabolic Research, 43, no. 8 (2011):524-530,
https://doi.org/10.1055/s-0031-1280784 .
17
16
17

Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats

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

(2011)

TY  - JOUR
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Stojiljković, Mojca D.
AU  - Milosavljević, Tijana
AU  - Isenović, Esma R.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4494
AB  - Background Fructose consumption produces deleterious metabolic effects in animal models. The sites of fructose-induced insulin resistance are documented to be the liver, skeletal muscle, and adipose tissue, but effects of fructose-rich diet on cardiac insulin signaling and action were not investigated. Purpose and methods In order to study the potential fructose effects on development of cardiac insulin resistance, we analyzed biochemical parameters relevant for insulin action and phosphorylation of insulin signaling molecules, plasma membrane glucose transporter type 4 (GLUT4) content, and phosphorylation of endothelial nitric oxide synthase (eNOS), in ovariectomized female rats on fructose-enriched diet, in basal and insulin-stimulated conditions. Results Fructose-fed rats (FFR) had increased content of visceral adipose tissue, but not body weight. Food intake was decreased, while fluid and caloric intake were increased in FFR. Additionally, fructose diet increased plasma insulin, blood triglycerides level, and HOMA index. Stimulation of protein kinase B (Akt) signaling pathway by insulin was reduced in rats on fructose-enriched diet, but effect of fructose on extracellular signal-regulated kinase (Erk 1/2) phosphorylation was not observed. Furthermore, insulin-induced GLUT4 presence in plasma membranes of cardiac cells was decreased by fructose diet, as well as insulin stimulation of eNOS phosphorylation at Ser(1177). Conclusion In summary, these results strongly support our hypothesis that fructose diet-induced changes of plasma lipid profile and insulin sensitivity are accompanied with decrease in cardiac insulin action in ovariectomized female rats.
T2  - European Journal of Nutrition
T1  - Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats
VL  - 50
IS  - 7
SP  - 543
EP  - 551
DO  - 10.1007/s00394-010-0161-4
ER  - 
@article{
author = "Žakula, Zorica and Korićanac, Goran and Tepavčević, Snežana and Stojiljković, Mojca D. and Milosavljević, Tijana and Isenović, Esma R.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4494",
abstract = "Background Fructose consumption produces deleterious metabolic effects in animal models. The sites of fructose-induced insulin resistance are documented to be the liver, skeletal muscle, and adipose tissue, but effects of fructose-rich diet on cardiac insulin signaling and action were not investigated. Purpose and methods In order to study the potential fructose effects on development of cardiac insulin resistance, we analyzed biochemical parameters relevant for insulin action and phosphorylation of insulin signaling molecules, plasma membrane glucose transporter type 4 (GLUT4) content, and phosphorylation of endothelial nitric oxide synthase (eNOS), in ovariectomized female rats on fructose-enriched diet, in basal and insulin-stimulated conditions. Results Fructose-fed rats (FFR) had increased content of visceral adipose tissue, but not body weight. Food intake was decreased, while fluid and caloric intake were increased in FFR. Additionally, fructose diet increased plasma insulin, blood triglycerides level, and HOMA index. Stimulation of protein kinase B (Akt) signaling pathway by insulin was reduced in rats on fructose-enriched diet, but effect of fructose on extracellular signal-regulated kinase (Erk 1/2) phosphorylation was not observed. Furthermore, insulin-induced GLUT4 presence in plasma membranes of cardiac cells was decreased by fructose diet, as well as insulin stimulation of eNOS phosphorylation at Ser(1177). Conclusion In summary, these results strongly support our hypothesis that fructose diet-induced changes of plasma lipid profile and insulin sensitivity are accompanied with decrease in cardiac insulin action in ovariectomized female rats.",
journal = "European Journal of Nutrition",
title = "Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats",
volume = "50",
number = "7",
pages = "543-551",
doi = "10.1007/s00394-010-0161-4"
}
Žakula, Z., Korićanac, G., Tepavčević, S., Stojiljković, M. D., Milosavljević, T.,& Isenović, E. R. (2011). Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats.
European Journal of Nutrition, 50(7), 543-551.
https://doi.org/10.1007/s00394-010-0161-4
Žakula Z, Korićanac G, Tepavčević S, Stojiljković MD, Milosavljević T, Isenović ER. Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats. European Journal of Nutrition. 2011;50(7):543-551
Žakula Zorica, Korićanac Goran, Tepavčević Snežana, Stojiljković Mojca D., Milosavljević Tijana, Isenović Esma R., "Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats" European Journal of Nutrition, 50, no. 7 (2011):543-551,
https://doi.org/10.1007/s00394-010-0161-4 .
18
20
22

Impact of estradiol on insulin signaling in the rat heart

Korićanac, Goran; Milosavljević, Tijana; Stojiljković, Mojca D.; Žakula, Zorica; Tepavčević, Snežana; Ribarac-Stepić, Nevena B.; Isenović, Esma R.

(2009)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Žakula, Zorica
AU  - Tepavčević, Snežana
AU  - Ribarac-Stepić, Nevena B.
AU  - Isenović, Esma R.
PY  - 2009
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3648
AB  - It is well known that variation in the concentration of estrogens affects insulin action. In this study we examine the impact of estradiol (E2) on insulin signaling in the rat heart. Ovariectomized female rats were treated with E2 6 h prior to analysis of basal protein and mRNA content of insulin signaling molecules, and additionally with insulin 30 min before the experiment to delineate E2 effects on phosphorylations and molecular associations relevant for insulin signaling. The results show that E2 decreased insulin receptor (IR) tyrosine phosphorylation, while it did not alter IR protein and mRNA content. E2 administration did not chance IR substrate 1 (IRS-1) protein content and tyrosine phosphorylation, while decreased mRNA content and increased its association with the p85 subunit of phosphatidylinositol 3-kinase (PI3K). E2 decreased protein and mRNA content of IR substrate 2 (IRS-2), while did not change IRS-2 tyrosine phosphorylation and IRS-2 association with p85. The increase of IRS-1/p85 is accompanied by increase of p85 protein and mRNA levels, and by stimulation of protein kinase B (Akt) Ser(473) phosphorylation. In contrast, Akt protein and mRNA content were not changed. In summary, although in some aspects cardiac insulin signaling is obviously improved by E2 treatment (increase of p85 mRNA and protein levels, enhancement of IRS-1/p85 association and Ser(473) Akt phosphorylation), the observed decrease of IR tyrosine phosphorylation, IRS-2 protein content, and IRSs mRNA contents, suggest very complex interplay of beneficial and suppressive effects of E2, both genomic and non-genomic, in regulation of heart insulin signaling. Copyright (C) 2009 John Wiley and Sons, Ltd.
T2  - Cell Biochemistry and Function
T1  - Impact of estradiol on insulin signaling in the rat heart
VL  - 27
IS  - 2
SP  - 102
EP  - 110
DO  - 10.1002/cbf.1542
ER  - 
@article{
author = "Korićanac, Goran and Milosavljević, Tijana and Stojiljković, Mojca D. and Žakula, Zorica and Tepavčević, Snežana and Ribarac-Stepić, Nevena B. and Isenović, Esma R.",
year = "2009",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3648",
abstract = "It is well known that variation in the concentration of estrogens affects insulin action. In this study we examine the impact of estradiol (E2) on insulin signaling in the rat heart. Ovariectomized female rats were treated with E2 6 h prior to analysis of basal protein and mRNA content of insulin signaling molecules, and additionally with insulin 30 min before the experiment to delineate E2 effects on phosphorylations and molecular associations relevant for insulin signaling. The results show that E2 decreased insulin receptor (IR) tyrosine phosphorylation, while it did not alter IR protein and mRNA content. E2 administration did not chance IR substrate 1 (IRS-1) protein content and tyrosine phosphorylation, while decreased mRNA content and increased its association with the p85 subunit of phosphatidylinositol 3-kinase (PI3K). E2 decreased protein and mRNA content of IR substrate 2 (IRS-2), while did not change IRS-2 tyrosine phosphorylation and IRS-2 association with p85. The increase of IRS-1/p85 is accompanied by increase of p85 protein and mRNA levels, and by stimulation of protein kinase B (Akt) Ser(473) phosphorylation. In contrast, Akt protein and mRNA content were not changed. In summary, although in some aspects cardiac insulin signaling is obviously improved by E2 treatment (increase of p85 mRNA and protein levels, enhancement of IRS-1/p85 association and Ser(473) Akt phosphorylation), the observed decrease of IR tyrosine phosphorylation, IRS-2 protein content, and IRSs mRNA contents, suggest very complex interplay of beneficial and suppressive effects of E2, both genomic and non-genomic, in regulation of heart insulin signaling. Copyright (C) 2009 John Wiley and Sons, Ltd.",
journal = "Cell Biochemistry and Function",
title = "Impact of estradiol on insulin signaling in the rat heart",
volume = "27",
number = "2",
pages = "102-110",
doi = "10.1002/cbf.1542"
}
Korićanac, G., Milosavljević, T., Stojiljković, M. D., Žakula, Z., Tepavčević, S., Ribarac-Stepić, N. B.,& Isenović, E. R. (2009). Impact of estradiol on insulin signaling in the rat heart.
Cell Biochemistry and Function, 27(2), 102-110.
https://doi.org/10.1002/cbf.1542
Korićanac G, Milosavljević T, Stojiljković MD, Žakula Z, Tepavčević S, Ribarac-Stepić NB, Isenović ER. Impact of estradiol on insulin signaling in the rat heart. Cell Biochemistry and Function. 2009;27(2):102-110
Korićanac Goran, Milosavljević Tijana, Stojiljković Mojca D., Žakula Zorica, Tepavčević Snežana, Ribarac-Stepić Nevena B., Isenović Esma R., "Impact of estradiol on insulin signaling in the rat heart" Cell Biochemistry and Function, 27, no. 2 (2009):102-110,
https://doi.org/10.1002/cbf.1542 .
15
18
19

Effects of dexamethasone on insulin receptor in aging

Korićanac, Goran; Stojiljković, Mojca D.; Radivojša, Snežana; Žakula, Zorica; Ribarac-Stepić, Nevena B.; Isenović, Esma R.

(2008)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Stojiljković, Mojca D.
AU  - Radivojša, Snežana
AU  - Žakula, Zorica
AU  - Ribarac-Stepić, Nevena B.
AU  - Isenović, Esma R.
PY  - 2008
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3365
AB  - The aim of this study was to examine the effects of dexamethasone (Dex) on functional properties of the rat insulin receptor (IR). Male Mill Hill hooded rats, 3, 6, 12, 18 and 21 months old, were injected with Dex (4 mg/kg) and rat liver and erythrocytes were used for experiments 18 h after Dex administration. Treatment with Dex lowered the specific binding (SB) of insulin ( INS) in the liver of 3- and 18-month-old rats and concentration of INS binding sites (N-1, N-2) and the dissociation constant of low-affinity binding sites (Kd(2)) in the liver of 6- and 18-month-old rats. In addition, Dex treatment lowered the liver IR protein level in all analyzed groups, except 21-month-old rats where it remained unchanged, but raised the IR mRNA level in 18-month-old rats. In erythrocytes, treatment with Dex decreased SB and Kd2 ( in animals 3 and 6 months old) and N1 ( in ones 3 and 18 months old). Following Dex treatment, the INS plasma level increased ( in rats 3, 18 and 21 months old), while glucose (Glu) concentration increased in 3 and 12 months old, but decreased in 6- and 21-month-old rats. In summary, Dex exerts the strongest effect on the erythrocyte IR of 3- and 6- month-old rats and the hepatic IR of 18-month-old rats. IR in both tissues is almost insensitive to Dex in 12- and 21-month-old rats. The pattern of age-related changes of IR induced by Dex does not correlate with changes of plasma Glu and INS.
T2  - Acta Biologica Hungarica
T1  - Effects of dexamethasone on insulin receptor in aging
VL  - 59
IS  - 1
SP  - 17
EP  - 29
DO  - 10.1556/ABiol.59.2008.1.2
ER  - 
@article{
author = "Korićanac, Goran and Stojiljković, Mojca D. and Radivojša, Snežana and Žakula, Zorica and Ribarac-Stepić, Nevena B. and Isenović, Esma R.",
year = "2008",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3365",
abstract = "The aim of this study was to examine the effects of dexamethasone (Dex) on functional properties of the rat insulin receptor (IR). Male Mill Hill hooded rats, 3, 6, 12, 18 and 21 months old, were injected with Dex (4 mg/kg) and rat liver and erythrocytes were used for experiments 18 h after Dex administration. Treatment with Dex lowered the specific binding (SB) of insulin ( INS) in the liver of 3- and 18-month-old rats and concentration of INS binding sites (N-1, N-2) and the dissociation constant of low-affinity binding sites (Kd(2)) in the liver of 6- and 18-month-old rats. In addition, Dex treatment lowered the liver IR protein level in all analyzed groups, except 21-month-old rats where it remained unchanged, but raised the IR mRNA level in 18-month-old rats. In erythrocytes, treatment with Dex decreased SB and Kd2 ( in animals 3 and 6 months old) and N1 ( in ones 3 and 18 months old). Following Dex treatment, the INS plasma level increased ( in rats 3, 18 and 21 months old), while glucose (Glu) concentration increased in 3 and 12 months old, but decreased in 6- and 21-month-old rats. In summary, Dex exerts the strongest effect on the erythrocyte IR of 3- and 6- month-old rats and the hepatic IR of 18-month-old rats. IR in both tissues is almost insensitive to Dex in 12- and 21-month-old rats. The pattern of age-related changes of IR induced by Dex does not correlate with changes of plasma Glu and INS.",
journal = "Acta Biologica Hungarica",
title = "Effects of dexamethasone on insulin receptor in aging",
volume = "59",
number = "1",
pages = "17-29",
doi = "10.1556/ABiol.59.2008.1.2"
}
Korićanac, G., Stojiljković, M. D., Radivojša, S., Žakula, Z., Ribarac-Stepić, N. B.,& Isenović, E. R. (2008). Effects of dexamethasone on insulin receptor in aging.
Acta Biologica Hungarica, 59(1), 17-29.
https://doi.org/10.1556/ABiol.59.2008.1.2
Korićanac G, Stojiljković MD, Radivojša S, Žakula Z, Ribarac-Stepić NB, Isenović ER. Effects of dexamethasone on insulin receptor in aging. Acta Biologica Hungarica. 2008;59(1):17-29
Korićanac Goran, Stojiljković Mojca D., Radivojša Snežana, Žakula Zorica, Ribarac-Stepić Nevena B., Isenović Esma R., "Effects of dexamethasone on insulin receptor in aging" Acta Biologica Hungarica, 59, no. 1 (2008):17-29,
https://doi.org/10.1556/ABiol.59.2008.1.2 .
2
2
2

Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol

Korićanac, Goran; Milosavljević, Tijana; Stojiljković, Mojca D.; Žakula, Zorica; Ribarac-Stepić, Nevena B.; Isenović, Esma R.

(2008)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Žakula, Zorica
AU  - Ribarac-Stepić, Nevena B.
AU  - Isenović, Esma R.
PY  - 2008
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3378
AB  - We used rat hepatic and uterine tissues to examine the impact of estradiol (E2) on insulin (INS) signaling. Ovariectotnized (OVX) female Wistar rats were treated with E2 (20 mu g/kg b.wt., i.p.) and used for the experiment 6 h after E2 administration. To highlight E2 effects on tyrosine phosphorylation of INS receptor (IR) and INS receptor substrates (IRSs) and IRSs association with p85 subunit of phosphatidylinositol 3-kinase (PI3-K) in the context of INS signaling, E2-treated OVX rats were also injected with INS (20 IU, i.p.), 30 min before the experiment. Treatment with E2 did not change the levels of plasma INS and glucose (Glu). However, it significantly decreased the free fatty acid (FFA) level and increased uterine weight. Furthermore, the results show that E2 had no effect on the content of hepatic IR protein, but significantly increased IR protein content in the uterus and decreased IR tyrosine phosphorylation in both the liver and uterus. Compared to the control, hepatic IRS-1 and IRS-2 were significantly decreased and increased, respectively, after E2 treatment. Protein content of both molecules, IRS-1 and IRS-2, was increased in uterine tissue after E2 administration. Protein content of the p85 subunit of PI3-K and that of protein kinase B (Akt) were increased in the uterus, with no changes in the liver. The results suggest that E2 treatment induces tissue-specific changes in INS signaling. The consequences of E2 treatment on INS signaling molecules are more apparent in the uterus, but their physiological relevance for INS action is probably greater in the liver. (c) 2007 Elsevier Ltd. All rights reserved.
T2  - Journal of Steroid Biochemistry and Molecular Biology
T1  - Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol
VL  - 108
IS  - 1-2
SP  - 109
EP  - 116
DO  - 10.1016/j.jsbmb.2007.06.001
ER  - 
@article{
author = "Korićanac, Goran and Milosavljević, Tijana and Stojiljković, Mojca D. and Žakula, Zorica and Ribarac-Stepić, Nevena B. and Isenović, Esma R.",
year = "2008",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3378",
abstract = "We used rat hepatic and uterine tissues to examine the impact of estradiol (E2) on insulin (INS) signaling. Ovariectotnized (OVX) female Wistar rats were treated with E2 (20 mu g/kg b.wt., i.p.) and used for the experiment 6 h after E2 administration. To highlight E2 effects on tyrosine phosphorylation of INS receptor (IR) and INS receptor substrates (IRSs) and IRSs association with p85 subunit of phosphatidylinositol 3-kinase (PI3-K) in the context of INS signaling, E2-treated OVX rats were also injected with INS (20 IU, i.p.), 30 min before the experiment. Treatment with E2 did not change the levels of plasma INS and glucose (Glu). However, it significantly decreased the free fatty acid (FFA) level and increased uterine weight. Furthermore, the results show that E2 had no effect on the content of hepatic IR protein, but significantly increased IR protein content in the uterus and decreased IR tyrosine phosphorylation in both the liver and uterus. Compared to the control, hepatic IRS-1 and IRS-2 were significantly decreased and increased, respectively, after E2 treatment. Protein content of both molecules, IRS-1 and IRS-2, was increased in uterine tissue after E2 administration. Protein content of the p85 subunit of PI3-K and that of protein kinase B (Akt) were increased in the uterus, with no changes in the liver. The results suggest that E2 treatment induces tissue-specific changes in INS signaling. The consequences of E2 treatment on INS signaling molecules are more apparent in the uterus, but their physiological relevance for INS action is probably greater in the liver. (c) 2007 Elsevier Ltd. All rights reserved.",
journal = "Journal of Steroid Biochemistry and Molecular Biology",
title = "Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol",
volume = "108",
number = "1-2",
pages = "109-116",
doi = "10.1016/j.jsbmb.2007.06.001"
}
Korićanac, G., Milosavljević, T., Stojiljković, M. D., Žakula, Z., Ribarac-Stepić, N. B.,& Isenović, E. R. (2008). Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol.
Journal of Steroid Biochemistry and Molecular Biology, 108(1-2), 109-116.
https://doi.org/10.1016/j.jsbmb.2007.06.001
Korićanac G, Milosavljević T, Stojiljković MD, Žakula Z, Ribarac-Stepić NB, Isenović ER. Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol. Journal of Steroid Biochemistry and Molecular Biology. 2008;108(1-2):109-116
Korićanac Goran, Milosavljević Tijana, Stojiljković Mojca D., Žakula Zorica, Ribarac-Stepić Nevena B., Isenović Esma R., "Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol" Journal of Steroid Biochemistry and Molecular Biology, 108, no. 1-2 (2008):109-116,
https://doi.org/10.1016/j.jsbmb.2007.06.001 .
15
16
17

Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor

Žakula, Zorica; Isenović, Esma R.; Stojiljković, Mojca D.; Tepavčević, Snežana; Ribarac-Stepić, Nevena B.

(2007)

TY  - JOUR
AU  - Žakula, Zorica
AU  - Isenović, Esma R.
AU  - Stojiljković, Mojca D.
AU  - Tepavčević, Snežana
AU  - Ribarac-Stepić, Nevena B.
PY  - 2007
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3412
AB  - The aim of this study was to examine the effects of estradiol (E2) on activity of RNA polymerase I and RNA polymerase II in uterine nuclei of ovariectomized (OVX) female rats. The obtained results show that estrogen-receptor (E-R) complexes in 30 min induced an increase of polymerase II activity. A second increase of polymerase II activity was observed after 3 h-incubation of nuclei with the E-R complex formed in the cytosol fraction. However, activity of polymerase I was increased 2 h after the start of incubation, with highest activity detected at 3 h in nuclei incubated with E-R complexes. On the contrary, no stimulatory effect on either polymerase I or polymerase II activity was observed in nuclei incubated with E2 alone. These results indicate that E2 stimulates the cytosolic estrogen receptor (ER), which in turn causes uterotrophic responses in OVX rats. In addition, they suggest that in order to provoke uterotrophic responses E-R complexes formed in the cytosol need to be retained in the nucleus for a longer period of time.
T2  - Archives of biological sciences
T1  - Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor
VL  - 59
IS  - 2
SP  - 105
EP  - 112
DO  - 10.2298/ABS0702105Z
ER  - 
@article{
author = "Žakula, Zorica and Isenović, Esma R. and Stojiljković, Mojca D. and Tepavčević, Snežana and Ribarac-Stepić, Nevena B.",
year = "2007",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3412",
abstract = "The aim of this study was to examine the effects of estradiol (E2) on activity of RNA polymerase I and RNA polymerase II in uterine nuclei of ovariectomized (OVX) female rats. The obtained results show that estrogen-receptor (E-R) complexes in 30 min induced an increase of polymerase II activity. A second increase of polymerase II activity was observed after 3 h-incubation of nuclei with the E-R complex formed in the cytosol fraction. However, activity of polymerase I was increased 2 h after the start of incubation, with highest activity detected at 3 h in nuclei incubated with E-R complexes. On the contrary, no stimulatory effect on either polymerase I or polymerase II activity was observed in nuclei incubated with E2 alone. These results indicate that E2 stimulates the cytosolic estrogen receptor (ER), which in turn causes uterotrophic responses in OVX rats. In addition, they suggest that in order to provoke uterotrophic responses E-R complexes formed in the cytosol need to be retained in the nucleus for a longer period of time.",
journal = "Archives of biological sciences",
title = "Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor",
volume = "59",
number = "2",
pages = "105-112",
doi = "10.2298/ABS0702105Z"
}
Žakula, Z., Isenović, E. R., Stojiljković, M. D., Tepavčević, S.,& Ribarac-Stepić, N. B. (2007). Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor.
Archives of biological sciences, 59(2), 105-112.
https://doi.org/10.2298/ABS0702105Z
Žakula Z, Isenović ER, Stojiljković MD, Tepavčević S, Ribarac-Stepić NB. Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor. Archives of biological sciences. 2007;59(2):105-112
Žakula Zorica, Isenović Esma R., Stojiljković Mojca D., Tepavčević Snežana, Ribarac-Stepić Nevena B., "Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor" Archives of biological sciences, 59, no. 2 (2007):105-112,
https://doi.org/10.2298/ABS0702105Z .

The effect of 17 beta-estradiol on the content of insulin signaling molecules in liver and uterus of ovariectomized rats

Korićanac, Goran; Vulović, Mojica; Milosavljevic, T; Žakula, Zorica; Ribarac-Stepić, Nevena B.

(2005)

TY  - CONF
AU  - Korićanac, Goran
AU  - Vulović, Mojica
AU  - Milosavljevic, T
AU  - Žakula, Zorica
AU  - Ribarac-Stepić, Nevena B.
PY  - 2005
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/6564
C3  - FEBS Journal
T1  - The effect of 17 beta-estradiol on the content of insulin signaling molecules in liver and uterus of ovariectomized rats
VL  - 272
SP  - 221
EP  - 222
ER  - 
@conference{
author = "Korićanac, Goran and Vulović, Mojica and Milosavljevic, T and Žakula, Zorica and Ribarac-Stepić, Nevena B.",
year = "2005",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/6564",
journal = "FEBS Journal",
title = "The effect of 17 beta-estradiol on the content of insulin signaling molecules in liver and uterus of ovariectomized rats",
volume = "272",
pages = "221-222"
}
Korićanac, G., Vulović, M., Milosavljevic, T., Žakula, Z.,& Ribarac-Stepić, N. B. (2005). The effect of 17 beta-estradiol on the content of insulin signaling molecules in liver and uterus of ovariectomized rats.
FEBS Journal, 272, 221-222.
Korićanac G, Vulović M, Milosavljevic T, Žakula Z, Ribarac-Stepić NB. The effect of 17 beta-estradiol on the content of insulin signaling molecules in liver and uterus of ovariectomized rats. FEBS Journal. 2005;272:221-222
Korićanac Goran, Vulović Mojica, Milosavljevic T, Žakula Zorica, Ribarac-Stepić Nevena B., "The effect of 17 beta-estradiol on the content of insulin signaling molecules in liver and uterus of ovariectomized rats" FEBS Journal, 272 (2005):221-222

Basal and glucocorticoid induced changes of hepatic glucocorticoid receptor during aging: relation to activities of tyrosine aminotransferase and tryptophan oxygenase

Ribarac-Stepić, Nevena B.; Vulović, Mojica; Korićanac, Goran; Isenović, Esma R.

(2005)

TY  - JOUR
AU  - Ribarac-Stepić, Nevena B.
AU  - Vulović, Mojica
AU  - Korićanac, Goran
AU  - Isenović, Esma R.
PY  - 2005
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/2908
AB  - The characteristics of glucocorticoid receptors, their sensitivity to glucocorticoid as well as the basal and glucocorticoid induced thyrosine aminotranferase (TAT) and tryptophan oxygenase (TO) activities were studied in rat liver during aging. The concentration (N) and dissociation constant (K-d) of glucocorticoid receptor (GR) significantly change during the aging both in untreated and dexamethasone treated animals. The level of receptors was lower in dexamethasone treated rats of all analyzed aged groups compared to untreated animals. In comparison to untreated groups, there was no correlation between the changes of N and K-d during the lifespan. According to immunochemical analysis, the decline of receptor protein content occurs during lifespan. Dexamethasone treatment reduced the level of receptor protein compare to respective age group of untreated rats. The glucocorticoid-receptor (G-R) complexes from both untreated and treated animals underwent thermal activation, although the extent of activation was more pronounced in the case of untreated groups compared to treated animals. The magnitude of heat activation of receptor complexes was more pronounced in the liver of the youngest untreated rats compared to elderly ones, while the receptor activation between treated groups of studied ages has shown less significant differences. Besides, basal as well as induced TAT and TO activities after dexamethasone injection also showed age-related alterations. The observed alterations in GR might play a role in the changes of the cell responses to glucocorticoid during the age. This presumption is supported by detected changes in basal and dexamethasone induced TAT and TO activities during aging.
T2  - Biogerontology
T1  - Basal and glucocorticoid induced changes of hepatic glucocorticoid receptor during aging: relation to activities of tyrosine aminotransferase and tryptophan oxygenase
VL  - 6
IS  - 2
SP  - 113
EP  - 131
DO  - 10.1007/s10522-005-3498-y
ER  - 
@article{
author = "Ribarac-Stepić, Nevena B. and Vulović, Mojica and Korićanac, Goran and Isenović, Esma R.",
year = "2005",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/2908",
abstract = "The characteristics of glucocorticoid receptors, their sensitivity to glucocorticoid as well as the basal and glucocorticoid induced thyrosine aminotranferase (TAT) and tryptophan oxygenase (TO) activities were studied in rat liver during aging. The concentration (N) and dissociation constant (K-d) of glucocorticoid receptor (GR) significantly change during the aging both in untreated and dexamethasone treated animals. The level of receptors was lower in dexamethasone treated rats of all analyzed aged groups compared to untreated animals. In comparison to untreated groups, there was no correlation between the changes of N and K-d during the lifespan. According to immunochemical analysis, the decline of receptor protein content occurs during lifespan. Dexamethasone treatment reduced the level of receptor protein compare to respective age group of untreated rats. The glucocorticoid-receptor (G-R) complexes from both untreated and treated animals underwent thermal activation, although the extent of activation was more pronounced in the case of untreated groups compared to treated animals. The magnitude of heat activation of receptor complexes was more pronounced in the liver of the youngest untreated rats compared to elderly ones, while the receptor activation between treated groups of studied ages has shown less significant differences. Besides, basal as well as induced TAT and TO activities after dexamethasone injection also showed age-related alterations. The observed alterations in GR might play a role in the changes of the cell responses to glucocorticoid during the age. This presumption is supported by detected changes in basal and dexamethasone induced TAT and TO activities during aging.",
journal = "Biogerontology",
title = "Basal and glucocorticoid induced changes of hepatic glucocorticoid receptor during aging: relation to activities of tyrosine aminotransferase and tryptophan oxygenase",
volume = "6",
number = "2",
pages = "113-131",
doi = "10.1007/s10522-005-3498-y"
}
Ribarac-Stepić, N. B., Vulović, M., Korićanac, G.,& Isenović, E. R. (2005). Basal and glucocorticoid induced changes of hepatic glucocorticoid receptor during aging: relation to activities of tyrosine aminotransferase and tryptophan oxygenase.
Biogerontology, 6(2), 113-131.
https://doi.org/10.1007/s10522-005-3498-y
Ribarac-Stepić NB, Vulović M, Korićanac G, Isenović ER. Basal and glucocorticoid induced changes of hepatic glucocorticoid receptor during aging: relation to activities of tyrosine aminotransferase and tryptophan oxygenase. Biogerontology. 2005;6(2):113-131
Ribarac-Stepić Nevena B., Vulović Mojica, Korićanac Goran, Isenović Esma R., "Basal and glucocorticoid induced changes of hepatic glucocorticoid receptor during aging: relation to activities of tyrosine aminotransferase and tryptophan oxygenase" Biogerontology, 6, no. 2 (2005):113-131,
https://doi.org/10.1007/s10522-005-3498-y .
9
6
9

Age-related changes of insulin receptors, plasma insulin and glucose level

Korićanac, Goran; Vulović, Mojica; Radivojša, Snežana; Žakula, Zorica; Ribarac-Stepić, Nevena B.

(2004)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Vulović, Mojica
AU  - Radivojša, Snežana
AU  - Žakula, Zorica
AU  - Ribarac-Stepić, Nevena B.
PY  - 2004
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/2827
AB  - The effects of aging on hepatic and erythrocyte insulin receptors have been investigated in 6, 12, 18 and 21-months-old compare to 3-months-old rats. Plasma insulin was elevated in 6, 12 and 18-months-old rats. Specific binding of insulin in liver was increased at the age of 18 months and accompanied with increase in concentration of low affinity binding sites, while specific binding to erythrocytes as well as concentration of both classes of binding sites was increased in 6-months-old rats. The protein and mRNA content of hepatic receptor were decreased only in the oldest animals. Plasma glucose was elevated starting from 12-months-old rats, while, after decrease in 6-months-old animals, citrulline was raised in the oldest group. The results demonstrating that specific binding of insulin in liver and erythrocytes and the concentration of binding sites in both tissues were not decreased during aging, as well as the absence of changes in affinity of insulin binding sites do not point out to occurrence of insulin resistance. However, the increase in insulinemia in the middle of lifespan, elevated plasma glucose and citrulline as well as decrease of hepatic receptor protein and mRNA content in the oldest animals indicate some age-related changes in insulin signaling.
T2  - Biogerontology
T1  - Age-related changes of insulin receptors, plasma insulin and glucose level
VL  - 5
IS  - 5
SP  - 345
EP  - 353
DO  - 10.1007/s10522-004-2576-x
ER  - 
@article{
author = "Korićanac, Goran and Vulović, Mojica and Radivojša, Snežana and Žakula, Zorica and Ribarac-Stepić, Nevena B.",
year = "2004",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/2827",
abstract = "The effects of aging on hepatic and erythrocyte insulin receptors have been investigated in 6, 12, 18 and 21-months-old compare to 3-months-old rats. Plasma insulin was elevated in 6, 12 and 18-months-old rats. Specific binding of insulin in liver was increased at the age of 18 months and accompanied with increase in concentration of low affinity binding sites, while specific binding to erythrocytes as well as concentration of both classes of binding sites was increased in 6-months-old rats. The protein and mRNA content of hepatic receptor were decreased only in the oldest animals. Plasma glucose was elevated starting from 12-months-old rats, while, after decrease in 6-months-old animals, citrulline was raised in the oldest group. The results demonstrating that specific binding of insulin in liver and erythrocytes and the concentration of binding sites in both tissues were not decreased during aging, as well as the absence of changes in affinity of insulin binding sites do not point out to occurrence of insulin resistance. However, the increase in insulinemia in the middle of lifespan, elevated plasma glucose and citrulline as well as decrease of hepatic receptor protein and mRNA content in the oldest animals indicate some age-related changes in insulin signaling.",
journal = "Biogerontology",
title = "Age-related changes of insulin receptors, plasma insulin and glucose level",
volume = "5",
number = "5",
pages = "345-353",
doi = "10.1007/s10522-004-2576-x"
}
Korićanac, G., Vulović, M., Radivojša, S., Žakula, Z.,& Ribarac-Stepić, N. B. (2004). Age-related changes of insulin receptors, plasma insulin and glucose level.
Biogerontology, 5(5), 345-353.
https://doi.org/10.1007/s10522-004-2576-x
Korićanac G, Vulović M, Radivojša S, Žakula Z, Ribarac-Stepić NB. Age-related changes of insulin receptors, plasma insulin and glucose level. Biogerontology. 2004;5(5):345-353
Korićanac Goran, Vulović Mojica, Radivojša Snežana, Žakula Zorica, Ribarac-Stepić Nevena B., "Age-related changes of insulin receptors, plasma insulin and glucose level" Biogerontology, 5, no. 5 (2004):345-353,
https://doi.org/10.1007/s10522-004-2576-x .
7
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