Effect of heat stress and bezafibrate on mitochondrial beta-oxidation: comparison between cultured cells from normal and mitochondrial fatty acid oxidation disorder children using in vitro probe acylcarnitine profiling assay.
Identifieur interne : 000331 ( Ncbi/Merge ); précédent : 000330; suivant : 000332Effect of heat stress and bezafibrate on mitochondrial beta-oxidation: comparison between cultured cells from normal and mitochondrial fatty acid oxidation disorder children using in vitro probe acylcarnitine profiling assay.
Auteurs : Hong Li [Japon] ; Seiji Fukuda ; Yuki Hasegawa ; Hironori Kobayashi ; Jamiyan Purevsuren ; Yuichi Mushimoto ; Seiji YamaguchiSource :
- Brain & development [ 1872-7131 ] ; 2010.
Descripteurs français
- KwdFr :
- Acides gras (), Acides gras (métabolisme), Acyl-CoA dehydrogenase (déficit), Bézafibrate (pharmacologie), Carnitine (), Carnitine (analogues et dérivés), Carnitine (métabolisme), Cellules cultivées, Enfant, Erreurs innées du métabolisme lipidique (génétique), Erreurs innées du métabolisme lipidique (métabolisme), Fibroblastes (), Fibroblastes (cytologie), Fibroblastes (métabolisme), Humains, Hypolipémiants (pharmacologie), Long-chain-acyl-CoA dehydrogenase (déficit), Maladies mitochondriales (génétique), Maladies mitochondriales (métabolisme), Mitochondries (), Mitochondries (métabolisme), Oxydoréduction (), Stress physiologique, Température élevée.
- MESH :
- analogues et dérivés : Carnitine.
- cytologie : Fibroblastes.
- déficit : Acyl-CoA dehydrogenase, Long-chain-acyl-CoA dehydrogenase.
- génétique : Erreurs innées du métabolisme lipidique, Maladies mitochondriales.
- métabolisme : Acides gras, Carnitine, Erreurs innées du métabolisme lipidique, Fibroblastes, Maladies mitochondriales, Mitochondries.
- pharmacologie : Bézafibrate, Hypolipémiants.
- Acides gras, Carnitine, Cellules cultivées, Enfant, Fibroblastes, Humains, Mitochondries, Oxydoréduction, Stress physiologique, Température élevée.
English descriptors
- KwdEn :
- Acyl-CoA Dehydrogenase (deficiency), Acyl-CoA Dehydrogenase, Long-Chain (deficiency), Bezafibrate (pharmacology), Carnitine (analogs & derivatives), Carnitine (chemistry), Carnitine (metabolism), Cells, Cultured, Child, Fatty Acids (chemistry), Fatty Acids (metabolism), Fibroblasts (cytology), Fibroblasts (drug effects), Fibroblasts (metabolism), Hot Temperature, Humans, Hypolipidemic Agents (pharmacology), Lipid Metabolism, Inborn Errors (genetics), Lipid Metabolism, Inborn Errors (metabolism), Mitochondria (drug effects), Mitochondria (metabolism), Mitochondrial Diseases (genetics), Mitochondrial Diseases (metabolism), Oxidation-Reduction (drug effects), Stress, Physiological.
- MESH :
- chemical , analogs & derivatives : Carnitine.
- chemical , chemistry : Carnitine, Fatty Acids.
- chemical , deficiency : Acyl-CoA Dehydrogenase, Acyl-CoA Dehydrogenase, Long-Chain.
- chemical , metabolism : Carnitine, Fatty Acids.
- chemical , pharmacology : Bezafibrate, Hypolipidemic Agents.
- cytology : Fibroblasts.
- drug effects : Fibroblasts, Mitochondria, Oxidation-Reduction.
- genetics : Lipid Metabolism, Inborn Errors, Mitochondrial Diseases.
- metabolism : Fibroblasts, Lipid Metabolism, Inborn Errors, Mitochondria, Mitochondrial Diseases.
- Cells, Cultured, Child, Hot Temperature, Humans, Stress, Physiological.
Abstract
Hyperpyrexia occasionally triggers acute life-threatening encephalopathy-like illnesses, including influenza-associated encephalopathy (IAE) in childhood, and can be responsible for impaired fatty acid beta-oxidation (FAO). In this regard, patients with impaired FAO may be more susceptible to febrile episodes. The effects of heat stress and a hypolipidemic drug, bezafibrate, on mitochondrial FAO were investigated using cultured cells from children with FAO disorders and from normal controls, using an in vitro probe acylcarnitine (AC) profiling assay. Fibroblasts were incubated in medium loaded with unlabelled palmitic acid for 96 h at 37 and 41 degrees C, with or without bezafibrate. AC profiles in culture medium were analyzed by electrospray ionization tandem mass spectrometry. Heat stress, introduced by 41 degrees C, significantly increased acetylcarnitine (C2) but slightly decreased the other acylcarnitines (ACs) in controls and medium-chain acyl-CoA dehydrogenase (MCAD)-deficient cells. On the other hand, in very long-chain acyl-CoA dehydrogenase (VLCAD)-deficient cells, accumulation of long-chain ACs were enhanced at 41 degrees C, compared with that at 37 degrees C. In contrast, bezafibrate decreased long-chain ACs with significant increase of C2 in both control and VLCAD-deficient cells at 37 degrees C. These data suggest that heat stress specifically inhibits long-chain FAO, whereas bezafibrate recovers the impaired FAO. Our approach is a simple and promising strategy to evaluate the effects of heat stress or therapeutic drugs on mitochondrial FAO.
DOI: 10.1016/j.braindev.2009.06.001
PubMed: 19589653
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000732
- to stream PubMed, to step Curation: 000729
- to stream PubMed, to step Checkpoint: 000690
Links to Exploration step
pubmed:19589653Le document en format XML
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sort="Yamaguchi, Seiji" uniqKey="Yamaguchi S" first="Seiji" last="Yamaguchi">Seiji Yamaguchi</name></author></analytic><series><title level="j">Brain & development</title><idno type="eISSN">1872-7131</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acyl-CoA Dehydrogenase (deficiency)</term><term>Acyl-CoA Dehydrogenase, Long-Chain (deficiency)</term><term>Bezafibrate (pharmacology)</term><term>Carnitine (analogs & derivatives)</term><term>Carnitine (chemistry)</term><term>Carnitine (metabolism)</term><term>Cells, Cultured</term><term>Child</term><term>Fatty Acids (chemistry)</term><term>Fatty Acids (metabolism)</term><term>Fibroblasts (cytology)</term><term>Fibroblasts (drug effects)</term><term>Fibroblasts (metabolism)</term><term>Hot Temperature</term><term>Humans</term><term>Hypolipidemic Agents (pharmacology)</term><term>Lipid Metabolism, Inborn Errors (genetics)</term><term>Lipid Metabolism, Inborn Errors (metabolism)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Mitochondrial Diseases (genetics)</term><term>Mitochondrial Diseases (metabolism)</term><term>Oxidation-Reduction (drug effects)</term><term>Stress, Physiological</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acides gras ()</term><term>Acides gras (métabolisme)</term><term>Acyl-CoA dehydrogenase (déficit)</term><term>Bézafibrate (pharmacologie)</term><term>Carnitine ()</term><term>Carnitine (analogues et dérivés)</term><term>Carnitine (métabolisme)</term><term>Cellules cultivées</term><term>Enfant</term><term>Erreurs innées du métabolisme lipidique (génétique)</term><term>Erreurs innées du métabolisme lipidique (métabolisme)</term><term>Fibroblastes ()</term><term>Fibroblastes (cytologie)</term><term>Fibroblastes (métabolisme)</term><term>Humains</term><term>Hypolipémiants (pharmacologie)</term><term>Long-chain-acyl-CoA dehydrogenase (déficit)</term><term>Maladies mitochondriales (génétique)</term><term>Maladies mitochondriales (métabolisme)</term><term>Mitochondries ()</term><term>Mitochondries (métabolisme)</term><term>Oxydoréduction ()</term><term>Stress physiologique</term><term>Température élevée</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Carnitine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Carnitine</term><term>Fatty Acids</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Acyl-CoA Dehydrogenase</term><term>Acyl-CoA Dehydrogenase, Long-Chain</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carnitine</term><term>Fatty Acids</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Bezafibrate</term><term>Hypolipidemic Agents</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Carnitine</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Fibroblastes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Fibroblasts</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Fibroblasts</term><term>Mitochondria</term><term>Oxidation-Reduction</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Acyl-CoA dehydrogenase</term><term>Long-chain-acyl-CoA dehydrogenase</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lipid Metabolism, Inborn Errors</term><term>Mitochondrial Diseases</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Erreurs innées du métabolisme lipidique</term><term>Maladies mitochondriales</term></keywords><keywords 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physiologique</term><term>Température élevée</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hyperpyrexia occasionally triggers acute life-threatening encephalopathy-like illnesses, including influenza-associated encephalopathy (IAE) in childhood, and can be responsible for impaired fatty acid beta-oxidation (FAO). In this regard, patients with impaired FAO may be more susceptible to febrile episodes. The effects of heat stress and a hypolipidemic drug, bezafibrate, on mitochondrial FAO were investigated using cultured cells from children with FAO disorders and from normal controls, using an in vitro probe acylcarnitine (AC) profiling assay. Fibroblasts were incubated in medium loaded with unlabelled palmitic acid for 96 h at 37 and 41 degrees C, with or without bezafibrate. AC profiles in culture medium were analyzed by electrospray ionization tandem mass spectrometry. Heat stress, introduced by 41 degrees C, significantly increased acetylcarnitine (C2) but slightly decreased the other acylcarnitines (ACs) in controls and medium-chain acyl-CoA dehydrogenase (MCAD)-deficient cells. On the other hand, in very long-chain acyl-CoA dehydrogenase (VLCAD)-deficient cells, accumulation of long-chain ACs were enhanced at 41 degrees C, compared with that at 37 degrees C. In contrast, bezafibrate decreased long-chain ACs with significant increase of C2 in both control and VLCAD-deficient cells at 37 degrees C. These data suggest that heat stress specifically inhibits long-chain FAO, whereas bezafibrate recovers the impaired FAO. Our approach is a simple and promising strategy to evaluate the effects of heat stress or therapeutic drugs on mitochondrial FAO.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19589653</PMID><DateCompleted><Year>2010</Year><Month>06</Month><Day>24</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7131</ISSN><JournalIssue CitedMedium="Internet"><Volume>32</Volume><Issue>5</Issue><PubDate><Year>2010</Year><Month>May</Month></PubDate></JournalIssue><Title>Brain & development</Title><ISOAbbreviation>Brain Dev.</ISOAbbreviation></Journal><ArticleTitle>Effect of heat stress and bezafibrate on mitochondrial beta-oxidation: comparison between cultured cells from normal and mitochondrial fatty acid oxidation disorder children using in vitro probe acylcarnitine profiling assay.</ArticleTitle><Pagination><MedlinePgn>362-70</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.braindev.2009.06.001</ELocationID><Abstract><AbstractText>Hyperpyrexia occasionally triggers acute life-threatening encephalopathy-like illnesses, including influenza-associated encephalopathy (IAE) in childhood, and can be responsible for impaired fatty acid beta-oxidation (FAO). In this regard, patients with impaired FAO may be more susceptible to febrile episodes. The effects of heat stress and a hypolipidemic drug, bezafibrate, on mitochondrial FAO were investigated using cultured cells from children with FAO disorders and from normal controls, using an in vitro probe acylcarnitine (AC) profiling assay. Fibroblasts were incubated in medium loaded with unlabelled palmitic acid for 96 h at 37 and 41 degrees C, with or without bezafibrate. AC profiles in culture medium were analyzed by electrospray ionization tandem mass spectrometry. Heat stress, introduced by 41 degrees C, significantly increased acetylcarnitine (C2) but slightly decreased the other acylcarnitines (ACs) in controls and medium-chain acyl-CoA dehydrogenase (MCAD)-deficient cells. On the other hand, in very long-chain acyl-CoA dehydrogenase (VLCAD)-deficient cells, accumulation of long-chain ACs were enhanced at 41 degrees C, compared with that at 37 degrees C. In contrast, bezafibrate decreased long-chain ACs with significant increase of C2 in both control and VLCAD-deficient cells at 37 degrees C. These data suggest that heat stress specifically inhibits long-chain FAO, whereas bezafibrate recovers the impaired FAO. Our approach is a simple and promising strategy to evaluate the effects of heat stress or therapeutic drugs on mitochondrial FAO.</AbstractText><CopyrightInformation>Copyright 2009 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Hong</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Shimane University School of Medicine, Izumo, Shimane, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fukuda</LastName><ForeName>Seiji</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Hasegawa</LastName><ForeName>Yuki</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Kobayashi</LastName><ForeName>Hironori</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Purevsuren</LastName><ForeName>Jamiyan</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Mushimoto</LastName><ForeName>Yuichi</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Yamaguchi</LastName><ForeName>Seiji</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>07</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Brain Dev</MedlineTA><NlmUniqueID>7909235</NlmUniqueID><ISSNLinking>0387-7604</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005227">Fatty Acids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000960">Hypolipidemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C116917">acylcarnitine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.3.8.7</RegistryNumber><NameOfSubstance UI="D042964">Acyl-CoA Dehydrogenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.3.8.8</RegistryNumber><NameOfSubstance UI="D044942">Acyl-CoA Dehydrogenase, Long-Chain</NameOfSubstance></Chemical><Chemical><RegistryNumber>S7UI8SM58A</RegistryNumber><NameOfSubstance UI="D002331">Carnitine</NameOfSubstance></Chemical><Chemical><RegistryNumber>Y9449Q51XH</RegistryNumber><NameOfSubstance UI="D001629">Bezafibrate</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D042964" MajorTopicYN="N">Acyl-CoA Dehydrogenase</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044942" MajorTopicYN="N">Acyl-CoA Dehydrogenase, Long-Chain</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001629" MajorTopicYN="N">Bezafibrate</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002331" MajorTopicYN="N">Carnitine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005227" MajorTopicYN="Y">Fatty Acids</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006358" MajorTopicYN="Y">Hot Temperature</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000960" MajorTopicYN="N">Hypolipidemic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008052" MajorTopicYN="N">Lipid Metabolism, Inborn Errors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="Y">Mitochondria</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D028361" MajorTopicYN="N">Mitochondrial Diseases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2009</Year><Month>01</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2009</Year><Month>05</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>06</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>7</Month><Day>11</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>7</Month><Day>11</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19589653</ArticleId><ArticleId IdType="pii">S0387-7604(09)00170-3</ArticleId><ArticleId IdType="doi">10.1016/j.braindev.2009.06.001</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Fukuda, Seiji" sort="Fukuda, Seiji" uniqKey="Fukuda S" first="Seiji" last="Fukuda">Seiji Fukuda</name><name sortKey="Hasegawa, Yuki" sort="Hasegawa, Yuki" uniqKey="Hasegawa Y" first="Yuki" last="Hasegawa">Yuki Hasegawa</name><name sortKey="Kobayashi, Hironori" sort="Kobayashi, Hironori" uniqKey="Kobayashi H" first="Hironori" last="Kobayashi">Hironori Kobayashi</name><name sortKey="Mushimoto, Yuichi" sort="Mushimoto, Yuichi" uniqKey="Mushimoto Y" first="Yuichi" last="Mushimoto">Yuichi Mushimoto</name><name sortKey="Purevsuren, Jamiyan" sort="Purevsuren, Jamiyan" uniqKey="Purevsuren J" first="Jamiyan" last="Purevsuren">Jamiyan Purevsuren</name><name sortKey="Yamaguchi, Seiji" sort="Yamaguchi, Seiji" uniqKey="Yamaguchi S" first="Seiji" last="Yamaguchi">Seiji Yamaguchi</name></noCountry><country name="Japon"><noRegion><name sortKey="Li, Hong" sort="Li, Hong" uniqKey="Li H" first="Hong" last="Li">Hong Li</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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}}
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HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/RBID.i -Sk "pubmed:19589653" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd \
| NlmPubMed2Wicri -a StressCovidV1
| This area was generated with Dilib version V0.6.33. |  |