Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet
Само за регистроване кориснике
2016
Аутори
Stanišić, JelenaKorićanac, Goran
Ćulafić, Tijana
Romić, Snježana Đ.
Stojiljković, Mojca D.
Kostić, Milan
Pantelić, Marija
Tepavčević, Snežana
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
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.
Кључне речи:
Low intensity exercise / Fructose / Heart / Insulin signaling pathway / Insulin resistance / Endothelial nitric oxide synthaseИзвор:
Molecular and Cellular Endocrinology, 2016, 420, C, 97-104Издавач:
- Elsevier
Финансирање / 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)
DOI: 10.1016/j.mce.2015.11.032
ISSN: 0303-7207
PubMed: 26644274
WoS: 000368949700010
Scopus: 2-s2.0-84949557272
Колекције
Институција/група
VinčaTY - 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 - https://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. PB - Elsevier 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", 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.", publisher = "Elsevier", 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. in Molecular and Cellular Endocrinology Elsevier., 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. in Molecular and Cellular Endocrinology. 2016;420(C):97-104. doi:10.1016/j.mce.2015.11.032 .
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" in Molecular and Cellular Endocrinology, 420, no. C (2016):97-104, https://doi.org/10.1016/j.mce.2015.11.032 . .