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Modulation of cardiac connexin-43 by omega-3 fatty acid ethyl-ester supplementation demonstrated in spontaneously diabetic rats
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SYSNO ASEP 0454188 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Modulation of cardiac connexin-43 by omega-3 fatty acid ethyl-ester supplementation demonstrated in spontaneously diabetic rats Author(s) Radošinská, J. (SK)
Kurahara, L. H. (JP)
Hiraishi, K. (JP)
Viczenczová, C. (SK)
Egan Beňová, T. (SK)
Szeiffová Bačová, B. (SK)
Dosenko, V. (UA)
Navarová, J. (SK)
Obšitník, B. (SK)
Imanaga, I. (JP)
Soukup, Tomáš (FGU-C) RID
Tribulová, N. (SK)Source Title Physiological Research. - : Fyziologický ústav AV ČR, v. v. i. - ISSN 0862-8408
Roč. 64, č. 6 (2015), s. 795-806Number of pages 12 s. Language eng - English Country CZ - Czech Republic Keywords diabetes ; omega-3 fatty acids ; cardiac connexin-43 ; PKC ; ultrastructure Subject RIV ED - Physiology R&D Projects 7AMB14SK123 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) Institutional support FGU-C - RVO:67985823 UT WOS 000367547900002 EID SCOPUS 84983212602 Annotation Omega-3 intake reduced blood glucose, triglycerides, and cholesterol in diabetic rats and this was associated with improved integrity of cardiomyocytes and capillaries in the heart. Myocardial Cx43 mRNA and protein levels were higher in diabetic versus non-diabetic rats and were further enhanced by omega-3. The ratio of phosphorylated (functional) to non-phosphorylated Cx43 was lower in diabetic compared to non-diabetic rats but was increased by omega-3, in part due to up-regulation of PKC-epsilon. Spontaneously diabetic rats at an early stage of disease benefit from omega-3 intake due to its hypoglycemic effect, upregulation of myocardial Cx43, and preservation of cardiovascular ultrastructure. These findings indicates that supplementation of omega-3 may be beneficial also in the management of diabetes in humans Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2016
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