Please use this identifier to cite or link to this item:https://hdl.handle.net/20.500.12512/78943
Type of publication: conference paper
Type of publication (PDB): Tezės Clarivate Analytics Web of Science ar/ir Scopus / Theses in Clarivate Analytics Web of Science and/or Scopus DB (T1a)
Field of Science: Medicina / Medicine (M001)
Author(s): Kopustinskienė, Dalia Marija;Polianskytė, Žydrūnė;Toleikis, Adolfas
Title: Accumulation of long chain fatty acids decreases the cardioprotective effect of KATP channel openers
Is part of: The FEBS journal : 30th FEBS congress and 9th IUBMB conference "The protein World" : abstracts : Budapest, Hungary, 2-7 July 2005. Oxford, UK : Published by Blackwell Pub. on behalf of the Federation of European Biochemical Societies, 2005, vol. 272, suppl. 1, July
Extent: p. 57-57, no. N5-013P
Date: 2005
Series/Report no.: (Abstracts)
Note: eISSN 1742-464X
Keywords: Fatty acids;Mitochondria, heart;physiology;KATP channels
Abstract: The oxidation of fatty acids serves as the main energy source for cardiomyocytes. However, in ischemic tissue fatty acid oxidation is inhibited, resulting in accumulation of long chain fatty acids and their CoA derivatives. In this study, we investigated the influence of fatty acids on the effects of KATP channel openers on isolated rat heart mitochondria. Mitochondrial respiration rates were recorded by the means of Clark-type oxygen electrode in the isotonic KCl medium (37 °C), using pyruvate and malate (6–6 mm) or fatty acids - palmitoyl-L-carnitine (9 mkm) and malate (240 mkm) or palmitoyl-CoA (5 mkm; + L-carnitine (2 mm)) and malate (240 mkm) as substrates. The results showed that KATP channel openers diazoxide (300 mkm) and pinacidil (300 mkm) similarly increased (by ~100%) the state 2 respiration rate of mitochondria, oxidizing either pyruvate and malate or fatty acids. In contrast, when palmitoyl-CoA (2.5 mkm) was not oxidized (medium devoid of carnitine), it suppressed the uncoupling effect of KATP channel openers in mitochondria, respiring on pyruvate and malate. Thus, during ischemia, the effects of KATP channel openers could decrease due to accumulation of physiological inhibitor of adenine nucleotide translocase - palmitoyl-CoA. Since uncoupling is proposed as one of the mechanisms of pharmacological cardioprotection, our results suggest that higher concentrations of KATP channel openers might be required to protect cardiomyocytes from ischemic injuries
Internet: https://hdl.handle.net/20.500.12512/78943
Affiliation(s): Kauno medicinos universiteto Biomedicininių tyrimų institutas
Lietuvos sveikatos mokslų universitetas
Appears in Collections:Universiteto mokslo publikacijos / University Research Publications

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