TY - JOUR
T1 - Baicalein 5,6,7-trimethyl ether activates peroxisomal but not mitochondrial fatty acid β-oxidation
AU - Morita, Masa
AU - Kanai, M.
AU - Mizuno, S.
AU - Iwashima, M.
AU - Hayashi, T.
AU - Shimozawa, N.
AU - Suzuki, Y.
AU - Imanaka, T.
N1 - Funding Information:
Acknowledgements This research was supported in part by a Grant-in-Aid for FThe Research Committee for Ataxic Diseases_ of the Research on Measures for Intractable Diseases from the Ministry of Health, Labour and Welfare of Japan, and for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (18590049). Pacific Edit reviewed the manuscript prior to submission.
PY - 2008/6
Y1 - 2008/6
N2 - 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 (C24:0) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid (C16:0) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, C24:0β-oxidation was also activated by treatment with BTM but C16:0 β-oxidation was not. The C16:0 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.
AB - 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 (C24:0) β-oxidation in the fibroblasts was stimulated by treatment with BTM, except for Zellweger fibroblasts. In contrasts, palmitic acid (C16:0) β-oxidation was increased (2.8-fold) only in CACT-deficient fibroblasts. In U87 glioblastoma cells, C24:0β-oxidation was also activated by treatment with BTM but C16:0 β-oxidation was not. The C16:0 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.
UR - http://www.scopus.com/inward/record.url?scp=45849111823&partnerID=8YFLogxK
U2 - 10.1007/s10545-008-0857-2
DO - 10.1007/s10545-008-0857-2
M3 - 学術論文
C2 - 18470630
AN - SCOPUS:45849111823
SN - 0141-8955
VL - 31
SP - 442
EP - 449
JO - Journal of Inherited Metabolic Disease
JF - Journal of Inherited Metabolic Disease
IS - 3
ER -