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

Authorized Users Only
2016
Authors
Stanišić, Jelena
Korićanac, Goran
Ćulafić, Tijana
Romić, Snježana Đ.
Stojiljković, Mojca D.
Kostić, Milan
Pantelić, Marija
Tepavčević, Snežana
Article (Published version)
Metadata
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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.

Keywords:
Low intensity exercise / Fructose / Heart / Insulin signaling pathway / Insulin resistance / Endothelial nitric oxide synthase
Source:
Molecular and Cellular Endocrinology, 2016, 420, C, 97-104
Publisher:
  • Elsevier
Funding / projects:
  • Role of steroid hormones in neuroendocrine adaptation to stress and pathophysiology of metabolic syndrome - molecular mechanisms and clinical implications (RS-41009)

DOI: 10.1016/j.mce.2015.11.032

ISSN: 0303-7207

PubMed: 26644274

WoS: 000368949700010

Scopus: 2-s2.0-84949557272
[ Google Scholar ]
16
19
URI
https://vinar.vin.bg.ac.rs/handle/123456789/913
Collections
  • WoS Import
Institution/Community
Vinča
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  - 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 . .

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