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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


THE INFLUENCE OF UCP BLOCKADE ON THE ENDOTHELIAL DYSFUNCTION WITH 1 TYPE EXPERIMENTAL DIABETES MELLITUS
Abstract number: OW02-8

Prysyazhna1 O.D., Sagach1 V.F.

1O.O. Bogomoletz Institute of Physiology NAS of United kingdomraine, Kiev, United kingdomraine [email protected]

Aim: 

Contemporary studies indicate the significant role of uncoupling proteins (UCP) increased expression in the development of complications of diabetes mellitus. An increase of UCP expression leads to the proton leak growth and the reduction of the effectiveness of the mitochondrial respiratory chain work. These changes, in turn, lead to reduction of ATP synthesis and increase of the oxidative stress. The purpose of this work is to investigate the influence of inhibitor UCP genipin introduction on the indices of endothelial dysfunction in the rats with stz-induced diabetes mellitus.

Methods: 

Streptozotocin 50 mg/kg was intraperitoneally injected to male rats of the weight 180-220g to reproduce experimental model of diabetes mellitus I type. Endothelium-dependent reactions of aorta and coronary vessels of rats with experimental diabetes mellitus after the single intraperitoneal introduction 10 mg/kg of UCP blocker genipin were studied.

Results: 

Experimental diabetes mellitus leads to the appearance of endothelial dysfunction that is revealed by the essential disturbance of endothelium-dependent reactions of the aorta and the coronary vessels both. The genipin injection brings to the partial restoration of disrupted reactions. It points to the role of growth of UCP expression in the appearance of the endothelial dysfunction with I type diabetes mellitus.

Conclusion: 

The application of UCP blockers is the forward-looking method of angioprotection and curing the vascular complications of diabetes mellitus.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :OW02-8

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