Hyperthyroidism Evokes Myocardial Ceramide Accumulation
Background: Thyroid hormones (THs) are key regulators of cardiac physiology as well as modulators of different cellular signals including the sphingomyelin/ceramide pathway. The objective of this study was to examine the effect of hyperthyroidism on the metabolism of sphingolipids in the muscle hear...
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Cell Physiol Biochem Press GmbH & Co KG
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doaj-2f8e0dcc4f944598bc2f8f0f4b2e46272020-11-24T21:25:45ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782015-01-0135275576610.1159/000369735369735Hyperthyroidism Evokes Myocardial Ceramide AccumulationAgnieszka MikłoszBartłomiej ŁukaszukAdrian ChabowskiFilip RogowskiKrzysztof KurekMałgorzata Żendzian-PiotrowskaBackground: Thyroid hormones (THs) are key regulators of cardiac physiology as well as modulators of different cellular signals including the sphingomyelin/ceramide pathway. The objective of this study was to examine the effect of hyperthyroidism on the metabolism of sphingolipids in the muscle heart. Methods: Male Wistar rats were treated for 10 days with triiodothyronine (T3) at a dose of 50µg/100g of body weight. Animals were then anaesthetized and samples of the left ventricle were excised. Results: We have demonstrated that prolonged, in vivo, T3 treatment increased the content of sphinganine (SFA), sphingosine (SFO), ceramide (CER) and sphingomyelin (SM), but decreased the level of sphingosine-1-phosphate (S1P) in cardiac muscle. Accordingly, the changes in sphingolipids content were accompanied by a lesser activity of neutral sphingomyelinase and without significant changes in ceramidases activity. Hyperthyroidism also induced activation of AMP-activated protein kinase (AMPK) with subsequently increased expression of mitochondrial proteins: cytochrome c oxidase IV (COX IV), β-hydroxyacyl-CoA dehydrogenase (β-HAD), carnityne palmitoyltransferase I (CPT I) and nuclear peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α). Conclusions: We conclude that prolonged T3 treatment increases sphingolipids metabolism which is reflected by higher concentration of SFA and CER in heart muscle. Furthermore, hyperthyroidism-induced increase in heart sphingomyelin (SM) concentration might be one of the mechanisms underlying maintenance of CER at relatively low level by its conversion to SM together with decreased S1P content.http://www.karger.com/Article/FullText/369735HeartCeramideTriiodothyronineSphingolipidsMitochondrial proteinsFatty acids oxidation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Agnieszka Mikłosz Bartłomiej Łukaszuk Adrian Chabowski Filip Rogowski Krzysztof Kurek Małgorzata Żendzian-Piotrowska |
spellingShingle |
Agnieszka Mikłosz Bartłomiej Łukaszuk Adrian Chabowski Filip Rogowski Krzysztof Kurek Małgorzata Żendzian-Piotrowska Hyperthyroidism Evokes Myocardial Ceramide Accumulation Cellular Physiology and Biochemistry Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation |
author_facet |
Agnieszka Mikłosz Bartłomiej Łukaszuk Adrian Chabowski Filip Rogowski Krzysztof Kurek Małgorzata Żendzian-Piotrowska |
author_sort |
Agnieszka Mikłosz |
title |
Hyperthyroidism Evokes Myocardial Ceramide Accumulation |
title_short |
Hyperthyroidism Evokes Myocardial Ceramide Accumulation |
title_full |
Hyperthyroidism Evokes Myocardial Ceramide Accumulation |
title_fullStr |
Hyperthyroidism Evokes Myocardial Ceramide Accumulation |
title_full_unstemmed |
Hyperthyroidism Evokes Myocardial Ceramide Accumulation |
title_sort |
hyperthyroidism evokes myocardial ceramide accumulation |
publisher |
Cell Physiol Biochem Press GmbH & Co KG |
series |
Cellular Physiology and Biochemistry |
issn |
1015-8987 1421-9778 |
publishDate |
2015-01-01 |
description |
Background: Thyroid hormones (THs) are key regulators of cardiac physiology as well as modulators of different cellular signals including the sphingomyelin/ceramide pathway. The objective of this study was to examine the effect of hyperthyroidism on the metabolism of sphingolipids in the muscle heart. Methods: Male Wistar rats were treated for 10 days with triiodothyronine (T3) at a dose of 50µg/100g of body weight. Animals were then anaesthetized and samples of the left ventricle were excised. Results: We have demonstrated that prolonged, in vivo, T3 treatment increased the content of sphinganine (SFA), sphingosine (SFO), ceramide (CER) and sphingomyelin (SM), but decreased the level of sphingosine-1-phosphate (S1P) in cardiac muscle. Accordingly, the changes in sphingolipids content were accompanied by a lesser activity of neutral sphingomyelinase and without significant changes in ceramidases activity. Hyperthyroidism also induced activation of AMP-activated protein kinase (AMPK) with subsequently increased expression of mitochondrial proteins: cytochrome c oxidase IV (COX IV), β-hydroxyacyl-CoA dehydrogenase (β-HAD), carnityne palmitoyltransferase I (CPT I) and nuclear peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α). Conclusions: We conclude that prolonged T3 treatment increases sphingolipids metabolism which is reflected by higher concentration of SFA and CER in heart muscle. Furthermore, hyperthyroidism-induced increase in heart sphingomyelin (SM) concentration might be one of the mechanisms underlying maintenance of CER at relatively low level by its conversion to SM together with decreased S1P content. |
topic |
Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation |
url |
http://www.karger.com/Article/FullText/369735 |
work_keys_str_mv |
AT agnieszkamikłosz hyperthyroidismevokesmyocardialceramideaccumulation AT bartłomiejłukaszuk hyperthyroidismevokesmyocardialceramideaccumulation AT adrianchabowski hyperthyroidismevokesmyocardialceramideaccumulation AT filiprogowski hyperthyroidismevokesmyocardialceramideaccumulation AT krzysztofkurek hyperthyroidismevokesmyocardialceramideaccumulation AT małgorzatazendzianpiotrowska hyperthyroidismevokesmyocardialceramideaccumulation |
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