Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats
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Žakula, ZoricaKorićanac, Goran
Tepavčević, Snežana
Stojiljković, Mojca D.
Milosavljević, Tijana
Isenović, Esma R.
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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, bl...ood 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.
Keywords:
Fructose / Heart / Insulin resistance / Glucose transporter type 4 / Nitric oxide synthase type IIISource:
European Journal of Nutrition, 2011, 50, 7, 543-551Funding / projects:
- Role of steroid hormones in neuroendocrine adaptation to stress and pathophysiology of metabolic syndrome - molecular mechanisms and clinical implications (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41009)
- Hormonal regulation of expression and activity of the nitric oxide synthase and sodium-potassium pump in experimental models of insulin resistance, diabetes and cardiovascular disorders (RS-MESTD-Basic Research (BR or ON)-173033)
DOI: 10.1007/s00394-010-0161-4
ISSN: 1436-6207; 1436-6215
PubMed: 21197538
WoS: 000295167700005
Scopus: 2-s2.0-79959813501
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VinčaTY - JOUR AU - Žakula, Zorica AU - Korićanac, Goran AU - Tepavčević, Snežana AU - Stojiljković, Mojca D. AU - Milosavljević, Tijana AU - Isenović, Esma R. PY - 2011 UR - https://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", 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. in 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. in European Journal of Nutrition. 2011;50(7):543-551. doi:10.1007/s00394-010-0161-4 .
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" in European Journal of Nutrition, 50, no. 7 (2011):543-551, https://doi.org/10.1007/s00394-010-0161-4 . .