Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation
Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal an...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Morita, M. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2008 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer Science+Business Media B.V. 2008 |
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| Übergeordnetes Werk: |
Enthalten in: Journal of inherited metabolic disease - Hoboken, NJ : Wiley, 1978, 31(2008), 3 vom: 09. Mai, Seite 442-449 |
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| Übergeordnetes Werk: |
volume:31 ; year:2008 ; number:3 ; day:09 ; month:05 ; pages:442-449 |
| Links: |
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| DOI / URN: |
10.1007/s10545-008-0857-2 |
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| Katalog-ID: |
SPR01136906X |
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| 041 | |a eng | ||
| 100 | 1 | |a Morita, M. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation |
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| 520 | |a Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. | ||
| 650 | 4 | |a Baicalein |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Zellweger Syndrome |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Lignoceric Acid |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a VLCFA Level |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a FATP4 Gene |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Kanai, M. |4 aut | |
| 700 | 1 | |a Mizuno, S. |4 aut | |
| 700 | 1 | |a Iwashima, M. |4 aut | |
| 700 | 1 | |a Hayashi, T. |4 aut | |
| 700 | 1 | |a Shimozawa, N. |4 aut | |
| 700 | 1 | |a Suzuki, Y. |4 aut | |
| 700 | 1 | |a Imanaka, T. |4 aut | |
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10.1007/s10545-008-0857-2 doi (DE-627)SPR01136906X (SPR)s10545-008-0857-2-e DE-627 ger DE-627 rakwb eng Morita, M. verfasserin aut Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media B.V. 2008 Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. Baicalein (dpeaa)DE-He213 Zellweger Syndrome (dpeaa)DE-He213 Lignoceric Acid (dpeaa)DE-He213 VLCFA Level (dpeaa)DE-He213 FATP4 Gene (dpeaa)DE-He213 Kanai, M. aut Mizuno, S. aut Iwashima, M. aut Hayashi, T. aut Shimozawa, N. aut Suzuki, Y. aut Imanaka, T. aut Enthalten in Journal of inherited metabolic disease Hoboken, NJ : Wiley, 1978 31(2008), 3 vom: 09. Mai, Seite 442-449 (DE-627)320457753 (DE-600)2006875-X 1573-2665 nnns volume:31 year:2008 number:3 day:09 month:05 pages:442-449 https://dx.doi.org/10.1007/s10545-008-0857-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2008 3 09 05 442-449 |
| spelling |
10.1007/s10545-008-0857-2 doi (DE-627)SPR01136906X (SPR)s10545-008-0857-2-e DE-627 ger DE-627 rakwb eng Morita, M. verfasserin aut Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media B.V. 2008 Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. Baicalein (dpeaa)DE-He213 Zellweger Syndrome (dpeaa)DE-He213 Lignoceric Acid (dpeaa)DE-He213 VLCFA Level (dpeaa)DE-He213 FATP4 Gene (dpeaa)DE-He213 Kanai, M. aut Mizuno, S. aut Iwashima, M. aut Hayashi, T. aut Shimozawa, N. aut Suzuki, Y. aut Imanaka, T. aut Enthalten in Journal of inherited metabolic disease Hoboken, NJ : Wiley, 1978 31(2008), 3 vom: 09. Mai, Seite 442-449 (DE-627)320457753 (DE-600)2006875-X 1573-2665 nnns volume:31 year:2008 number:3 day:09 month:05 pages:442-449 https://dx.doi.org/10.1007/s10545-008-0857-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2008 3 09 05 442-449 |
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10.1007/s10545-008-0857-2 doi (DE-627)SPR01136906X (SPR)s10545-008-0857-2-e DE-627 ger DE-627 rakwb eng Morita, M. verfasserin aut Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media B.V. 2008 Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. Baicalein (dpeaa)DE-He213 Zellweger Syndrome (dpeaa)DE-He213 Lignoceric Acid (dpeaa)DE-He213 VLCFA Level (dpeaa)DE-He213 FATP4 Gene (dpeaa)DE-He213 Kanai, M. aut Mizuno, S. aut Iwashima, M. aut Hayashi, T. aut Shimozawa, N. aut Suzuki, Y. aut Imanaka, T. aut Enthalten in Journal of inherited metabolic disease Hoboken, NJ : Wiley, 1978 31(2008), 3 vom: 09. Mai, Seite 442-449 (DE-627)320457753 (DE-600)2006875-X 1573-2665 nnns volume:31 year:2008 number:3 day:09 month:05 pages:442-449 https://dx.doi.org/10.1007/s10545-008-0857-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2008 3 09 05 442-449 |
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10.1007/s10545-008-0857-2 doi (DE-627)SPR01136906X (SPR)s10545-008-0857-2-e DE-627 ger DE-627 rakwb eng Morita, M. verfasserin aut Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media B.V. 2008 Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. Baicalein (dpeaa)DE-He213 Zellweger Syndrome (dpeaa)DE-He213 Lignoceric Acid (dpeaa)DE-He213 VLCFA Level (dpeaa)DE-He213 FATP4 Gene (dpeaa)DE-He213 Kanai, M. aut Mizuno, S. aut Iwashima, M. aut Hayashi, T. aut Shimozawa, N. aut Suzuki, Y. aut Imanaka, T. aut Enthalten in Journal of inherited metabolic disease Hoboken, NJ : Wiley, 1978 31(2008), 3 vom: 09. Mai, Seite 442-449 (DE-627)320457753 (DE-600)2006875-X 1573-2665 nnns volume:31 year:2008 number:3 day:09 month:05 pages:442-449 https://dx.doi.org/10.1007/s10545-008-0857-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2008 3 09 05 442-449 |
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10.1007/s10545-008-0857-2 doi (DE-627)SPR01136906X (SPR)s10545-008-0857-2-e DE-627 ger DE-627 rakwb eng Morita, M. verfasserin aut Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media B.V. 2008 Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. Baicalein (dpeaa)DE-He213 Zellweger Syndrome (dpeaa)DE-He213 Lignoceric Acid (dpeaa)DE-He213 VLCFA Level (dpeaa)DE-He213 FATP4 Gene (dpeaa)DE-He213 Kanai, M. aut Mizuno, S. aut Iwashima, M. aut Hayashi, T. aut Shimozawa, N. aut Suzuki, Y. aut Imanaka, T. aut Enthalten in Journal of inherited metabolic disease Hoboken, NJ : Wiley, 1978 31(2008), 3 vom: 09. Mai, Seite 442-449 (DE-627)320457753 (DE-600)2006875-X 1573-2665 nnns volume:31 year:2008 number:3 day:09 month:05 pages:442-449 https://dx.doi.org/10.1007/s10545-008-0857-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2008 3 09 05 442-449 |
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Enthalten in Journal of inherited metabolic disease 31(2008), 3 vom: 09. Mai, Seite 442-449 volume:31 year:2008 number:3 day:09 month:05 pages:442-449 |
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Enthalten in Journal of inherited metabolic disease 31(2008), 3 vom: 09. Mai, Seite 442-449 volume:31 year:2008 number:3 day:09 month:05 pages:442-449 |
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Baicalein Zellweger Syndrome Lignoceric Acid VLCFA Level FATP4 Gene |
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Morita, M. @@aut@@ Kanai, M. @@aut@@ Mizuno, S. @@aut@@ Iwashima, M. @@aut@@ Hayashi, T. @@aut@@ Shimozawa, N. @@aut@@ Suzuki, Y. @@aut@@ Imanaka, T. @@aut@@ |
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The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. 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|
| author |
Morita, M. |
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Morita, M. misc Baicalein misc Zellweger Syndrome misc Lignoceric Acid misc VLCFA Level misc FATP4 Gene Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation |
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Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation Baicalein (dpeaa)DE-He213 Zellweger Syndrome (dpeaa)DE-He213 Lignoceric Acid (dpeaa)DE-He213 VLCFA Level (dpeaa)DE-He213 FATP4 Gene (dpeaa)DE-He213 |
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misc Baicalein misc Zellweger Syndrome misc Lignoceric Acid misc VLCFA Level misc FATP4 Gene |
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misc Baicalein misc Zellweger Syndrome misc Lignoceric Acid misc VLCFA Level misc FATP4 Gene |
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Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation |
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Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation |
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Morita, M. |
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Journal of inherited metabolic disease |
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Morita, M. Kanai, M. Mizuno, S. Iwashima, M. Hayashi, T. Shimozawa, N. Suzuki, Y. Imanaka, T. |
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Morita, M. |
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10.1007/s10545-008-0857-2 |
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baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation |
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Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation |
| abstract |
Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. © Springer Science+Business Media B.V. 2008 |
| abstractGer |
Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. © Springer Science+Business Media B.V. 2008 |
| abstract_unstemmed |
Summary Recently, we reported that baicalein 5,6,7-trimethyl ether (BTM), a flavonoid, is capable of activating fatty acid β-oxidation in X-linked adrenoleukodystrophy (X-ALD) fibroblasts (FEBS Lett. 2005; 579: 409–414). The objective of this study was to clarify whether BTM activates peroxisomal and/or mitochondrial fatty acid β-oxidation. We first analysed the effect of BTM on fatty acid β-oxidation in fibroblasts derived from healthy controls as well as patients with X-ALD, mitochondrial carnitine-acylcarnitine translocase (CACT) deficiency, and peroxisome biogenesis disorder, Zellweger syndrome. Lignoceric acid ($ C_{24:0} $) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid ($ C_{16:0} $) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, $ C_{24:0} $ β-oxidation was also activated by treatment with BTM but $ C_{16:0} $ β-oxidation was not. The $ C_{16:0} $ β-oxidation was, however, significantly increased in the presence of 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA), a carnitine palmitoyltransferase I inhibitor. These results indicate that BTM activates peroxisomal but not mitochondrial fatty acid β-oxidation. In addition, we found that BTM did not upregulate the expression of ABCD2/ALDR, ABCD3/PMP70, ACOX1 and FATP4 genes but slightly increased ACSVL1 gene expression. © Springer Science+Business Media B.V. 2008 |
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| title_short |
Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation |
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https://dx.doi.org/10.1007/s10545-008-0857-2 |
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Kanai, M. Mizuno, S. Iwashima, M. Hayashi, T. Shimozawa, N. Suzuki, Y. Imanaka, T. |
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Kanai, M. Mizuno, S. Iwashima, M. Hayashi, T. Shimozawa, N. Suzuki, Y. Imanaka, T. |
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10.1007/s10545-008-0857-2 |
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2024-07-03T22:13:31.729Z |
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| score |
7.40047 |