Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Endothelial dysfunction in experimental models of metabolic syndrome − effect of fructose

Endothelial dysfunction in experimental models of metabolic syndrome − effect of fructose References[1] Anderson RA, Evans ML, Ellis GR, et al. The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes. Atherosclerosis 2001;154:475–483.[2] Bae JH, Bassenge E, Kim KB, et al. Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress. Atherosclerosis 2001;155:517–523.[3] Bartus M, Kostogrys RB, Kaÿmierczak P, et al. 1-Methylnicotinamide (MNA) prevents endothelial dysfunction in hypertriglyceridemic and diabetic rats. Pharmacol Rep. 2008;60:127–138.[4] Kaprinay B, Lipták B, Slovák L, et al. Hypertriglyceridemic rats fed high fat diet as a model of metabolic syndrome. Physiol Res. 2016; 65:S515-S518.[5] Kitagawa S, Sameshima E, Yamaguchi Y, Kwon Y, Shinozuka K, Kunitomo M. Comparison of the eff ects of hypercholesterolaemia on relaxation responses in aortas of spontaneously hypertensive rats and Dahl salt-sensitive rats. Clin Exp Pharmacol Physiol. 1995;22(suppl):S251-S253.10.1111/j.1440-1681.1995.tb02904.x[6] McCulloch AI, Bottrill FE, Randall MD, Hiley CR. Characterization and modulation of EDHF-mediated relaxations in the rat isolated superior mesenteric arterial bed. Br J Pharmacol.1997;120:1431-1438.[7] Miller AW, Hoenig ME, Ujhelyi MR. Mechanisms of Impaired Endothelial Function Associated with Insulin Resistance. J Cardiovasc Pharmacol Therapeut. 1998;3:125-133.[8] Pisulewski PM, Kostogrys RB, Lorkowska B, Bartuś M, Chłopicki S. Critical evaluation of normotensive rats as models for hypercholesterolaemia-induced atherosclerosis. J Anim Feed Sci. 2005;14:339-351.[9] Sasaki S, Yoneda Y, Fujita H, et al. Association of blood pressure variability with induction of atherosclerosis in cholesterol-fed rats. Am J Hypertens. 1994;7:453-459.10.1093/ajh/7.5.453[10] Sotnikova R, Bauer V. Nitric oxide production and its changes in diabetic endothelial dysfunction : chapter 7. Advances in molecular mechanisms and pharmacology of diabetic complications. In: Trivandrum : Transworld Research Networ. India, Kerala; 2010.[11] Van Oostrom AJ, Cabezas MC, Rabelink TJ. Insulin resistance and vessel endothelial function. J R Soc Med. 2002;95:54-61.[12] Young EJ, Hill MA, Wiehler WB, Triggle CR, Reid JJ. Reduced EDHF responses and connexin activity in mesenteric arteries from the insulin-resistant obese Zucker rat. Diabetologia2008;51:872-881. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Acta Facultatis Pharmaceuticae Universitatis Comenianae de Gruyter

Endothelial dysfunction in experimental models of metabolic syndrome − effect of fructose

Download PDF
3 pages

Loading next page...
 
/lp/de-gruyter/endothelial-dysfunction-in-experimental-models-of-metabolic-syndrome-tMyQZMQp0H

References (14)

Publisher
de Gruyter
Copyright
© 2017 Kaprinay B. et al., published by De Gruyter Open
ISSN
1338-6786
eISSN
2453-6725
DOI
10.1515/afpuc-2017-0014
Publisher site
See Article on Publisher Site

Abstract

References[1] Anderson RA, Evans ML, Ellis GR, et al. The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes. Atherosclerosis 2001;154:475–483.[2] Bae JH, Bassenge E, Kim KB, et al. Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress. Atherosclerosis 2001;155:517–523.[3] Bartus M, Kostogrys RB, Kaÿmierczak P, et al. 1-Methylnicotinamide (MNA) prevents endothelial dysfunction in hypertriglyceridemic and diabetic rats. Pharmacol Rep. 2008;60:127–138.[4] Kaprinay B, Lipták B, Slovák L, et al. Hypertriglyceridemic rats fed high fat diet as a model of metabolic syndrome. Physiol Res. 2016; 65:S515-S518.[5] Kitagawa S, Sameshima E, Yamaguchi Y, Kwon Y, Shinozuka K, Kunitomo M. Comparison of the eff ects of hypercholesterolaemia on relaxation responses in aortas of spontaneously hypertensive rats and Dahl salt-sensitive rats. Clin Exp Pharmacol Physiol. 1995;22(suppl):S251-S253.10.1111/j.1440-1681.1995.tb02904.x[6] McCulloch AI, Bottrill FE, Randall MD, Hiley CR. Characterization and modulation of EDHF-mediated relaxations in the rat isolated superior mesenteric arterial bed. Br J Pharmacol.1997;120:1431-1438.[7] Miller AW, Hoenig ME, Ujhelyi MR. Mechanisms of Impaired Endothelial Function Associated with Insulin Resistance. J Cardiovasc Pharmacol Therapeut. 1998;3:125-133.[8] Pisulewski PM, Kostogrys RB, Lorkowska B, Bartuś M, Chłopicki S. Critical evaluation of normotensive rats as models for hypercholesterolaemia-induced atherosclerosis. J Anim Feed Sci. 2005;14:339-351.[9] Sasaki S, Yoneda Y, Fujita H, et al. Association of blood pressure variability with induction of atherosclerosis in cholesterol-fed rats. Am J Hypertens. 1994;7:453-459.10.1093/ajh/7.5.453[10] Sotnikova R, Bauer V. Nitric oxide production and its changes in diabetic endothelial dysfunction : chapter 7. Advances in molecular mechanisms and pharmacology of diabetic complications. In: Trivandrum : Transworld Research Networ. India, Kerala; 2010.[11] Van Oostrom AJ, Cabezas MC, Rabelink TJ. Insulin resistance and vessel endothelial function. J R Soc Med. 2002;95:54-61.[12] Young EJ, Hill MA, Wiehler WB, Triggle CR, Reid JJ. Reduced EDHF responses and connexin activity in mesenteric arteries from the insulin-resistant obese Zucker rat. Diabetologia2008;51:872-881.

Journal

Acta Facultatis Pharmaceuticae Universitatis Comenianae – de Gruyter

Published: Sep 1, 2017

There are no references for this article.