Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?
Аутори
Romić, Snježana Đ.Tepavčević, Snežana
Žakula, Zorica
Milosavljević, Tijana
Stojiljković, Mojca D.
Živković, Maja
Popović, Milan
Stanković, Aleksandra
Korićanac, Goran
Чланак у часопису
Метаподаци
Приказ свих података о документуАпстракт
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-f...ed 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.
Кључне речи:
Fructose / Oestradiol / Heart / Protein kinase B / Endothelial nitric oxide synthaseИзвор:
British Journal of Nutrition, 2013, 109, 11, 1940-1948Финансирање / пројекти:
- Улога стероидних хормона у неуроендокриној адаптацији на стрес и патофизиологији метаболичког синдрома - молекуларни механизми и клиничке импликације (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41009)
- Генетска основа хуманих васкуларних и инфламаторних болести (RS-MESTD-Basic Research (BR or ON)-175085)
DOI: 10.1017/S0007114512004114
ISSN: 0007-1145
PubMed: 23069112
WoS: 000319126700003
Scopus: 2-s2.0-84877995385
Колекције
Институција/група
VinčaTY - 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 - https://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", 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?. in 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?. in British Journal of Nutrition. 2013;109(11):1940-1948. doi:10.1017/S0007114512004114 .
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?" in British Journal of Nutrition, 109, no. 11 (2013):1940-1948, https://doi.org/10.1017/S0007114512004114 . .