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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Autor*in:	Agnieszka Mikłosz [verfasserIn] Bartłomiej Łukaszuk [verfasserIn] Adrian Chabowski [verfasserIn] Filip Rogowski [verfasserIn] Krzysztof Kurek [verfasserIn] Małgorzata Żendzian-Piotrowska [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation

Übergeordnetes Werk:	In: Cellular Physiology and Biochemistry - Cell Physiol Biochem Press GmbH & Co KG, 2002, 35(2015), 2, Seite 755-766
Übergeordnetes Werk:	volume:35 ; year:2015 ; number:2 ; pages:755-766

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1159/000369735

Katalog-ID:	DOAJ006552676

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520			\|a 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.
650		4	\|a Heart
650		4	\|a Ceramide
650		4	\|a Triiodothyronine
650		4	\|a Sphingolipids
650		4	\|a Mitochondrial proteins
650		4	\|a Fatty acids oxidation
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allfields	10.1159/000369735 doi (DE-627)DOAJ006552676 (DE-599)DOAJ2f8e0dcc4f944598bc2f8f0f4b2e4627 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Agnieszka Mikłosz verfasserin aut Hyperthyroidism Evokes Myocardial Ceramide Accumulation 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation Physiology Biochemistry Bartłomiej Łukaszuk verfasserin aut Adrian Chabowski verfasserin aut Filip Rogowski verfasserin aut Krzysztof Kurek verfasserin aut Małgorzata Żendzian-Piotrowska verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 2, Seite 755-766 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:2 pages:755-766 https://doi.org/10.1159/000369735 kostenfrei https://doaj.org/article/2f8e0dcc4f944598bc2f8f0f4b2e4627 kostenfrei http://www.karger.com/Article/FullText/369735 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 2 755-766
spelling	10.1159/000369735 doi (DE-627)DOAJ006552676 (DE-599)DOAJ2f8e0dcc4f944598bc2f8f0f4b2e4627 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Agnieszka Mikłosz verfasserin aut Hyperthyroidism Evokes Myocardial Ceramide Accumulation 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation Physiology Biochemistry Bartłomiej Łukaszuk verfasserin aut Adrian Chabowski verfasserin aut Filip Rogowski verfasserin aut Krzysztof Kurek verfasserin aut Małgorzata Żendzian-Piotrowska verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 2, Seite 755-766 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:2 pages:755-766 https://doi.org/10.1159/000369735 kostenfrei https://doaj.org/article/2f8e0dcc4f944598bc2f8f0f4b2e4627 kostenfrei http://www.karger.com/Article/FullText/369735 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 2 755-766
allfields_unstemmed	10.1159/000369735 doi (DE-627)DOAJ006552676 (DE-599)DOAJ2f8e0dcc4f944598bc2f8f0f4b2e4627 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Agnieszka Mikłosz verfasserin aut Hyperthyroidism Evokes Myocardial Ceramide Accumulation 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation Physiology Biochemistry Bartłomiej Łukaszuk verfasserin aut Adrian Chabowski verfasserin aut Filip Rogowski verfasserin aut Krzysztof Kurek verfasserin aut Małgorzata Żendzian-Piotrowska verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 2, Seite 755-766 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:2 pages:755-766 https://doi.org/10.1159/000369735 kostenfrei https://doaj.org/article/2f8e0dcc4f944598bc2f8f0f4b2e4627 kostenfrei http://www.karger.com/Article/FullText/369735 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 2 755-766
allfieldsGer	10.1159/000369735 doi (DE-627)DOAJ006552676 (DE-599)DOAJ2f8e0dcc4f944598bc2f8f0f4b2e4627 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Agnieszka Mikłosz verfasserin aut Hyperthyroidism Evokes Myocardial Ceramide Accumulation 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation Physiology Biochemistry Bartłomiej Łukaszuk verfasserin aut Adrian Chabowski verfasserin aut Filip Rogowski verfasserin aut Krzysztof Kurek verfasserin aut Małgorzata Żendzian-Piotrowska verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 2, Seite 755-766 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:2 pages:755-766 https://doi.org/10.1159/000369735 kostenfrei https://doaj.org/article/2f8e0dcc4f944598bc2f8f0f4b2e4627 kostenfrei http://www.karger.com/Article/FullText/369735 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 2 755-766
allfieldsSound	10.1159/000369735 doi (DE-627)DOAJ006552676 (DE-599)DOAJ2f8e0dcc4f944598bc2f8f0f4b2e4627 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Agnieszka Mikłosz verfasserin aut Hyperthyroidism Evokes Myocardial Ceramide Accumulation 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation Physiology Biochemistry Bartłomiej Łukaszuk verfasserin aut Adrian Chabowski verfasserin aut Filip Rogowski verfasserin aut Krzysztof Kurek verfasserin aut Małgorzata Żendzian-Piotrowska verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 2, Seite 755-766 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:2 pages:755-766 https://doi.org/10.1159/000369735 kostenfrei https://doaj.org/article/2f8e0dcc4f944598bc2f8f0f4b2e4627 kostenfrei http://www.karger.com/Article/FullText/369735 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 2 755-766
language	English
source	In Cellular Physiology and Biochemistry 35(2015), 2, Seite 755-766 volume:35 year:2015 number:2 pages:755-766
sourceStr	In Cellular Physiology and Biochemistry 35(2015), 2, Seite 755-766 volume:35 year:2015 number:2 pages:755-766
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation Physiology Biochemistry
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container_title	Cellular Physiology and Biochemistry
authorswithroles_txt_mv	Agnieszka Mikłosz @@aut@@ Bartłomiej Łukaszuk @@aut@@ Adrian Chabowski @@aut@@ Filip Rogowski @@aut@@ Krzysztof Kurek @@aut@@ Małgorzata Żendzian-Piotrowska @@aut@@
publishDateDaySort_date	2015-01-01T00:00:00Z
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id	DOAJ006552676
language_de	englisch
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callnumber-first	Q - Science
author	Agnieszka Mikłosz
spellingShingle	Agnieszka Mikłosz misc QP1-981 misc QD415-436 misc Heart misc Ceramide misc Triiodothyronine misc Sphingolipids misc Mitochondrial proteins misc Fatty acids oxidation misc Physiology misc Biochemistry Hyperthyroidism Evokes Myocardial Ceramide Accumulation
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topic_title	QP1-981 QD415-436 Hyperthyroidism Evokes Myocardial Ceramide Accumulation Heart Ceramide Triiodothyronine Sphingolipids Mitochondrial proteins Fatty acids oxidation
topic	misc QP1-981 misc QD415-436 misc Heart misc Ceramide misc Triiodothyronine misc Sphingolipids misc Mitochondrial proteins misc Fatty acids oxidation misc Physiology misc Biochemistry
topic_unstemmed	misc QP1-981 misc QD415-436 misc Heart misc Ceramide misc Triiodothyronine misc Sphingolipids misc Mitochondrial proteins misc Fatty acids oxidation misc Physiology misc Biochemistry
topic_browse	misc QP1-981 misc QD415-436 misc Heart misc Ceramide misc Triiodothyronine misc Sphingolipids misc Mitochondrial proteins misc Fatty acids oxidation misc Physiology misc Biochemistry
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title	Hyperthyroidism Evokes Myocardial Ceramide Accumulation
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title_full	Hyperthyroidism Evokes Myocardial Ceramide Accumulation
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author_browse	Agnieszka Mikłosz Bartłomiej Łukaszuk Adrian Chabowski Filip Rogowski Krzysztof Kurek Małgorzata Żendzian-Piotrowska
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title_sort	hyperthyroidism evokes myocardial ceramide accumulation
callnumber	QP1-981
title_auth	Hyperthyroidism Evokes Myocardial Ceramide Accumulation
abstract	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.
abstractGer	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.
abstract_unstemmed	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.
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title_short	Hyperthyroidism Evokes Myocardial Ceramide Accumulation
url	https://doi.org/10.1159/000369735 https://doaj.org/article/2f8e0dcc4f944598bc2f8f0f4b2e4627 http://www.karger.com/Article/FullText/369735 https://doaj.org/toc/1015-8987 https://doaj.org/toc/1421-9778
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author2	Bartłomiej Łukaszuk Adrian Chabowski Filip Rogowski Krzysztof Kurek Małgorzata Żendzian-Piotrowska
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