Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats
Апстракт
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.
Кључне речи:
Nitric oxide synthase type III / Insulin resistance / Heart / Glucose transporter type 4 / FructoseИзвор:
European Journal of Nutrition, 2011, 50, 7, 543-551Финансирање / пројекти:
- Fig. 5 Effects of fructose-enriched diet on eNOS signaling in rat heart. Upper panels show representative Western blots for phosphorylation of eNOS at Ser1177 (peNOS) and total eNOS from rats on standard and fructose-rich diet in the absence or presence of insulin. Quantified ratio of peNOS/eNOS is shown in the lower panel. The abbreviations are the same as in Fig. 2. Values are given as means ± SD of three independent experiments with a total of seven animals per group. *p \ 0.05 vs. C; #p \ 0.05 vs. C ? INS. eNOS endothelial nitric oxide synthase, peNOS phospho-eNOS Acknowledgments This study was supported by the Project grant No. 41009 and No. 173033 (to E.R.I.) from the Ministry of Science and Technological Development, Republic of Serbia.
DOI: 10.1007/s00394-010-0161-4
ISSN: 1436-6207
PubMed: 21197538
WoS: 000295167700005
Scopus: 2-s2.0-79959813501
Институција/група
Institut za molekularnu genetiku i genetičko inženjerstvoTY - JOUR AU - Zakula, Z. AU - Koricanac, G. AU - Tepavcević, S. AU - Stojiljković, Mojca AU - Milosavljević, T. AU - Isenović, E.R. PY - 2011 UR - https://imagine.imgge.bg.ac.rs/handle/123456789/522 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 EP - 551 IS - 7 SP - 543 VL - 50 DO - 10.1007/s00394-010-0161-4 ER -
@article{ author = "Zakula, Z. and Koricanac, G. and Tepavcević, S. and Stojiljković, Mojca and Milosavljević, T. and Isenović, E.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", pages = "551-543", number = "7", volume = "50", doi = "10.1007/s00394-010-0161-4" }
Zakula, Z., Koricanac, G., Tepavcević, S., Stojiljković, M., 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
Zakula Z, Koricanac G, Tepavcević S, Stojiljković M, Milosavljević T, Isenović E. 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 .
Zakula, Z., Koricanac, G., Tepavcević, S., Stojiljković, Mojca, Milosavljević, T., Isenović, E.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 . .