EPA and DHA acylcarnitines are less cardiotoxic than are saturated and monounsaturated long‐chain acylcarnitines

Elevated levels of fatty acid‐derived long‐chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial function and key metabolic pathways in the heart. While trans‐fatty acids are considered harmful and omega‐3 polyunsaturated fatty acids (PUF...

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Veröffentlicht in:	BioFactors (Oxford) Jg. 51; H. 2; S. e70014 - n/a
Hauptverfasser:	Liepinsh, Edgars, Gukalova, Baiba, Krims‐Davis, Kristaps, Kuka, Janis, Leduskrasta, Aiga, Korzh, Stanislava, Vilskersts, Reinis, Makrecka‐Kuka, Marina, Konrade, Ilze, Dambrova, Maija
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Hoboken, USA John Wiley & Sons, Inc 01.03.2025
Schlagworte:	Animals Cardiotoxicity Carnitine - analogs & derivatives Carnitine - pharmacology Carnitine - toxicity Cell Survival - drug effects Docosahexaenoic Acids - pharmacology Docosahexaenoic Acids - toxicity Eicosapentaenoic Acid - analogs & derivatives Eicosapentaenoic Acid - pharmacology heart Insulin - metabolism mitochondria Mitochondria, Heart - drug effects Mitochondria, Heart - metabolism MUFA Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism omega‐3 PUFA Rats Signal Transduction - drug effects trans fatty acids unsaturated trans fatty acids omega‐3 PUFA mitochondria MUFA heart unsaturated
ISSN:	0951-6433, 1872-8081, 1872-8081
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Abstract	Elevated levels of fatty acid‐derived long‐chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial function and key metabolic pathways in the heart. While trans‐fatty acids are considered harmful and omega‐3 polyunsaturated fatty acids (PUFAs) are considered beneficial, the specific properties of acylcarnitines derived from these types of fatty acids are not characterized. This study aimed to compare the effects of saturated palmitoylcarnitine (PC), monounsaturated cis‐oleoylcarnitine (cis‐OC), trans‐elaidoylcarnitine (trans‐EC), and polyunsaturated eicosapentaenoylcarnitine (EPAC) and docosahexaenoylcarnitine (DHAC) on heart function, cardiac cell viability, mitochondrial functionality, and insulin signaling pathways. Saturated and monounsaturated acylcarnitines, particularly trans‐EC, significantly reduced cardiac contractility at concentrations of 8–12 μM, and trans‐EC was identified as the most cardiotoxic acylcarnitine. Conversely, the presence of EPAC and DHAC in the perfusion buffer did not impair heart functionality. Saturated and monounsaturated acylcarnitines also drastically reduced H9C2 cell viability and suppressed mitochondrial OXPHOS by up to 70% at 25 μM, whereas PUFA‐derived acylcarnitines caused only a 20%–25% reduction in OXPHOS and did not decrease cell viability. Furthermore, PC, cis‐OC, and trans‐EC significantly inhibited Akt phosphorylation, whereas EPAC and DHAC had a much weaker effect on insulin signaling. In conclusion, saturated and monounsaturated acylcarnitines, particularly trans‐EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega‐3 PUFA‐derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines. PUFA intake might be safer than other long‐chain fatty acid‐containing lipid sources in patients with FAODs and cardiometabolic diseases. Saturated and monounsaturated acylcarnitines, particularly trans‐EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega‐3 PUFA‐derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines.
AbstractList	Elevated levels of fatty acid‐derived long‐chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial function and key metabolic pathways in the heart. While trans‐fatty acids are considered harmful and omega‐3 polyunsaturated fatty acids (PUFAs) are considered beneficial, the specific properties of acylcarnitines derived from these types of fatty acids are not characterized. This study aimed to compare the effects of saturated palmitoylcarnitine (PC), monounsaturated cis‐oleoylcarnitine (cis‐OC), trans‐elaidoylcarnitine (trans‐EC), and polyunsaturated eicosapentaenoylcarnitine (EPAC) and docosahexaenoylcarnitine (DHAC) on heart function, cardiac cell viability, mitochondrial functionality, and insulin signaling pathways. Saturated and monounsaturated acylcarnitines, particularly trans‐EC, significantly reduced cardiac contractility at concentrations of 8–12 μM, and trans‐EC was identified as the most cardiotoxic acylcarnitine. Conversely, the presence of EPAC and DHAC in the perfusion buffer did not impair heart functionality. Saturated and monounsaturated acylcarnitines also drastically reduced H9C2 cell viability and suppressed mitochondrial OXPHOS by up to 70% at 25 μM, whereas PUFA‐derived acylcarnitines caused only a 20%–25% reduction in OXPHOS and did not decrease cell viability. Furthermore, PC, cis‐OC, and trans‐EC significantly inhibited Akt phosphorylation, whereas EPAC and DHAC had a much weaker effect on insulin signaling. In conclusion, saturated and monounsaturated acylcarnitines, particularly trans‐EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega‐3 PUFA‐derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines. PUFA intake might be safer than other long‐chain fatty acid‐containing lipid sources in patients with FAODs and cardiometabolic diseases. Elevated levels of fatty acid‐derived long‐chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial function and key metabolic pathways in the heart. While trans‐fatty acids are considered harmful and omega‐3 polyunsaturated fatty acids (PUFAs) are considered beneficial, the specific properties of acylcarnitines derived from these types of fatty acids are not characterized. This study aimed to compare the effects of saturated palmitoylcarnitine (PC), monounsaturated cis‐oleoylcarnitine (cis‐OC), trans‐elaidoylcarnitine (trans‐EC), and polyunsaturated eicosapentaenoylcarnitine (EPAC) and docosahexaenoylcarnitine (DHAC) on heart function, cardiac cell viability, mitochondrial functionality, and insulin signaling pathways. Saturated and monounsaturated acylcarnitines, particularly trans‐EC, significantly reduced cardiac contractility at concentrations of 8–12 μM, and trans‐EC was identified as the most cardiotoxic acylcarnitine. Conversely, the presence of EPAC and DHAC in the perfusion buffer did not impair heart functionality. Saturated and monounsaturated acylcarnitines also drastically reduced H9C2 cell viability and suppressed mitochondrial OXPHOS by up to 70% at 25 μM, whereas PUFA‐derived acylcarnitines caused only a 20%–25% reduction in OXPHOS and did not decrease cell viability. Furthermore, PC, cis‐OC, and trans‐EC significantly inhibited Akt phosphorylation, whereas EPAC and DHAC had a much weaker effect on insulin signaling. In conclusion, saturated and monounsaturated acylcarnitines, particularly trans‐EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega‐3 PUFA‐derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines. PUFA intake might be safer than other long‐chain fatty acid‐containing lipid sources in patients with FAODs and cardiometabolic diseases. Saturated and monounsaturated acylcarnitines, particularly trans‐EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega‐3 PUFA‐derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines. Elevated levels of fatty acid‐derived long‐chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial function and key metabolic pathways in the heart. While trans‐fatty acids are considered harmful and omega‐3 polyunsaturated fatty acids (PUFAs) are considered beneficial, the specific properties of acylcarnitines derived from these types of fatty acids are not characterized. This study aimed to compare the effects of saturated palmitoylcarnitine (PC), monounsaturated cis‐oleoylcarnitine (cis‐OC), trans‐elaidoylcarnitine (trans‐EC), and polyunsaturated eicosapentaenoylcarnitine (EPAC) and docosahexaenoylcarnitine (DHAC) on heart function, cardiac cell viability, mitochondrial functionality, and insulin signaling pathways. Saturated and monounsaturated acylcarnitines, particularly trans‐EC, significantly reduced cardiac contractility at concentrations of 8–12 μM, and trans‐EC was identified as the most cardiotoxic acylcarnitine. Conversely, the presence of EPAC and DHAC in the perfusion buffer did not impair heart functionality. Saturated and monounsaturated acylcarnitines also drastically reduced H9C2 cell viability and suppressed mitochondrial OXPHOS by up to 70% at 25 μM, whereas PUFA‐derived acylcarnitines caused only a 20%–25% reduction in OXPHOS and did not decrease cell viability. Furthermore, PC, cis‐OC, and trans‐EC significantly inhibited Akt phosphorylation, whereas EPAC and DHAC had a much weaker effect on insulin signaling. In conclusion, saturated and monounsaturated acylcarnitines, particularly trans‐EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega‐3 PUFA‐derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines. PUFA intake might be safer than other long‐chain fatty acid‐containing lipid sources in patients with FAODs and cardiometabolic diseases. Saturated and monounsaturated acylcarnitines, particularly trans‐EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega‐3 PUFA‐derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines. Elevated levels of fatty acid-derived long-chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial function and key metabolic pathways in the heart. While trans-fatty acids are considered harmful and omega-3 polyunsaturated fatty acids (PUFAs) are considered beneficial, the specific properties of acylcarnitines derived from these types of fatty acids are not characterized. This study aimed to compare the effects of saturated palmitoylcarnitine (PC), monounsaturated cis-oleoylcarnitine (cis-OC), trans-elaidoylcarnitine (trans-EC), and polyunsaturated eicosapentaenoylcarnitine (EPAC) and docosahexaenoylcarnitine (DHAC) on heart function, cardiac cell viability, mitochondrial functionality, and insulin signaling pathways. Saturated and monounsaturated acylcarnitines, particularly trans-EC, significantly reduced cardiac contractility at concentrations of 8-12 μM, and trans-EC was identified as the most cardiotoxic acylcarnitine. Conversely, the presence of EPAC and DHAC in the perfusion buffer did not impair heart functionality. Saturated and monounsaturated acylcarnitines also drastically reduced H9C2 cell viability and suppressed mitochondrial OXPHOS by up to 70% at 25 μM, whereas PUFA-derived acylcarnitines caused only a 20%-25% reduction in OXPHOS and did not decrease cell viability. Furthermore, PC, cis-OC, and trans-EC significantly inhibited Akt phosphorylation, whereas EPAC and DHAC had a much weaker effect on insulin signaling. In conclusion, saturated and monounsaturated acylcarnitines, particularly trans-EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega-3 PUFA-derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines. PUFA intake might be safer than other long-chain fatty acid-containing lipid sources in patients with FAODs and cardiometabolic diseases.Elevated levels of fatty acid-derived long-chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial function and key metabolic pathways in the heart. While trans-fatty acids are considered harmful and omega-3 polyunsaturated fatty acids (PUFAs) are considered beneficial, the specific properties of acylcarnitines derived from these types of fatty acids are not characterized. This study aimed to compare the effects of saturated palmitoylcarnitine (PC), monounsaturated cis-oleoylcarnitine (cis-OC), trans-elaidoylcarnitine (trans-EC), and polyunsaturated eicosapentaenoylcarnitine (EPAC) and docosahexaenoylcarnitine (DHAC) on heart function, cardiac cell viability, mitochondrial functionality, and insulin signaling pathways. Saturated and monounsaturated acylcarnitines, particularly trans-EC, significantly reduced cardiac contractility at concentrations of 8-12 μM, and trans-EC was identified as the most cardiotoxic acylcarnitine. Conversely, the presence of EPAC and DHAC in the perfusion buffer did not impair heart functionality. Saturated and monounsaturated acylcarnitines also drastically reduced H9C2 cell viability and suppressed mitochondrial OXPHOS by up to 70% at 25 μM, whereas PUFA-derived acylcarnitines caused only a 20%-25% reduction in OXPHOS and did not decrease cell viability. Furthermore, PC, cis-OC, and trans-EC significantly inhibited Akt phosphorylation, whereas EPAC and DHAC had a much weaker effect on insulin signaling. In conclusion, saturated and monounsaturated acylcarnitines, particularly trans-EC, exert significant cardiotoxic effects, primarily through the impairment of cardiac mitochondrial function. The omega-3 PUFA-derived acylcarnitines EPAC and DHAC are safe and less likely to damage cardiac mitochondria, cardiac cells, and the heart than other acylcarnitines. PUFA intake might be safer than other long-chain fatty acid-containing lipid sources in patients with FAODs and cardiometabolic diseases.
Author	Korzh, Stanislava Kuka, Janis Liepinsh, Edgars Vilskersts, Reinis Konrade, Ilze Gukalova, Baiba Leduskrasta, Aiga Krims‐Davis, Kristaps Makrecka‐Kuka, Marina Dambrova, Maija
AuthorAffiliation	1 Latvian Institute of Organic Synthesis Riga Latvia 3 Riga East Clinical Hospital Riga Latvia 2 Riga Stradins University Riga Latvia
AuthorAffiliation_xml	– name: 2 Riga Stradins University Riga Latvia – name: 3 Riga East Clinical Hospital Riga Latvia – name: 1 Latvian Institute of Organic Synthesis Riga Latvia
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Snippet	Elevated levels of fatty acid‐derived long‐chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial... Elevated levels of fatty acid-derived long-chain acylcarnitines are detrimental to cardiac health, primarily because of their adverse effects on mitochondrial...
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SubjectTerms	Animals Cardiotoxicity Carnitine - analogs & derivatives Carnitine - pharmacology Carnitine - toxicity Cell Survival - drug effects Docosahexaenoic Acids - pharmacology Docosahexaenoic Acids - toxicity Eicosapentaenoic Acid - analogs & derivatives Eicosapentaenoic Acid - pharmacology heart Insulin - metabolism mitochondria Mitochondria, Heart - drug effects Mitochondria, Heart - metabolism MUFA Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism omega‐3 PUFA Rats Signal Transduction - drug effects trans fatty acids unsaturated
Title	EPA and DHA acylcarnitines are less cardiotoxic than are saturated and monounsaturated long‐chain acylcarnitines
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