Nutritional regulation and role of peroxisome proliferator-activated receptor δ in fatty acid catabolism in skeletal muscle
Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors primarily involved in lipid homeostasis. PPARδ displays strong expression in tissues with high lipid metabolism, such as adipose, intestine and muscle. Its role in skeletal muscle remains largely unknown. After a 24-h starvati...
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| creator | Holst, Dorte Luquet, Serge Nogueira, Véronique Kristiansen, Karsten Leverve, Xavier Grimaldi, Paul A. |
| description | Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors primarily involved in lipid homeostasis. PPARδ displays strong expression in tissues with high lipid metabolism, such as adipose, intestine and muscle. Its role in skeletal muscle remains largely unknown. After a 24-h starvation period, PPARδ mRNA levels are dramatically up-regulated in gastrocnemius muscle of mice and restored to control level upon refeeding. The rise of PPARδ is accompanied by parallel up-regulations of fatty acid translocase/CD36 (FAT/CD36) and heart fatty acid binding protein (H-FABP), while refeeding promotes down-regulation of both genes. To directly access the role of PPARδ in muscle cells, we forced its expression and that of a dominant-negative PPARδ mutant in C2C12 myogenic cells. Differentiated C2C12 cells responds to 2-bromopalmitate or synthetic PPARδ agonist by induction of genes involved in lipid metabolism and increment of fatty acid oxidation. Overexpression of PPARδ enhanced these cellular responses, whereas expression of the dominant-negative mutant exerts opposite effects. These data strongly support a role for PPARδ in the regulation of fatty acid oxidation in skeletal muscle and in adaptive response of this tissue to lipid catabolism. |
| doi_str_mv | 10.1016/S1388-1981(03)00071-4 |
| format | Article |
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PPARδ displays strong expression in tissues with high lipid metabolism, such as adipose, intestine and muscle. Its role in skeletal muscle remains largely unknown. After a 24-h starvation period, PPARδ mRNA levels are dramatically up-regulated in gastrocnemius muscle of mice and restored to control level upon refeeding. The rise of PPARδ is accompanied by parallel up-regulations of fatty acid translocase/CD36 (FAT/CD36) and heart fatty acid binding protein (H-FABP), while refeeding promotes down-regulation of both genes. To directly access the role of PPARδ in muscle cells, we forced its expression and that of a dominant-negative PPARδ mutant in C2C12 myogenic cells. Differentiated C2C12 cells responds to 2-bromopalmitate or synthetic PPARδ agonist by induction of genes involved in lipid metabolism and increment of fatty acid oxidation. Overexpression of PPARδ enhanced these cellular responses, whereas expression of the dominant-negative mutant exerts opposite effects. These data strongly support a role for PPARδ in the regulation of fatty acid oxidation in skeletal muscle and in adaptive response of this tissue to lipid catabolism.</description><identifier>ISSN: 1388-1981</identifier><identifier>ISSN: 0006-3002</identifier><identifier>ISSN: 0167-4889</identifier><identifier>EISSN: 1879-2618</identifier><identifier>DOI: 10.1016/S1388-1981(03)00071-4</identifier><identifier>PMID: 12842194</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Biochemistry, Molecular Biology ; Carbon Radioisotopes ; Cell Differentiation ; Cell Differentiation - drug effects ; Cell Line ; Fatty acid ; Fatty acid oxidation ; Fatty Acids ; Fatty Acids - metabolism ; Gene expression ; Gene Expression Regulation ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - physiology ; Kinetics ; Life Sciences ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal ; Muscle, Skeletal - metabolism ; Mutation ; Myotube ; Nutritional Physiological Phenomena ; Palmitates ; Palmitates - pharmacology ; Receptors, Cytoplasmic and Nuclear ; Receptors, Cytoplasmic and Nuclear - agonists ; Receptors, Cytoplasmic and Nuclear - genetics ; Receptors, Cytoplasmic and Nuclear - metabolism ; RNA, Messenger ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Transcription Factors ; Transcription Factors - agonists ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transcriptional Activation</subject><ispartof>Biochimica et biophysica acta, 2003-07, Vol.1633 (1), p.43-50</ispartof><rights>2003 Elsevier B.V.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-70ce2be6cd54a275d7a80da2c4d780693e6c98986e35412457e79e13542bcb533</citedby><cites>FETCH-LOGICAL-c398t-70ce2be6cd54a275d7a80da2c4d780693e6c98986e35412457e79e13542bcb533</cites><orcidid>0000-0002-6024-0917 ; 0000-0001-8668-6645</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1388198103000714$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12842194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://inserm.hal.science/inserm-00389948$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Holst, Dorte</creatorcontrib><creatorcontrib>Luquet, Serge</creatorcontrib><creatorcontrib>Nogueira, Véronique</creatorcontrib><creatorcontrib>Kristiansen, Karsten</creatorcontrib><creatorcontrib>Leverve, Xavier</creatorcontrib><creatorcontrib>Grimaldi, Paul A.</creatorcontrib><title>Nutritional regulation and role of peroxisome proliferator-activated receptor δ in fatty acid catabolism in skeletal muscle</title><title>Biochimica et biophysica acta</title><addtitle>Biochim Biophys Acta</addtitle><description>Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors primarily involved in lipid homeostasis. PPARδ displays strong expression in tissues with high lipid metabolism, such as adipose, intestine and muscle. Its role in skeletal muscle remains largely unknown. After a 24-h starvation period, PPARδ mRNA levels are dramatically up-regulated in gastrocnemius muscle of mice and restored to control level upon refeeding. The rise of PPARδ is accompanied by parallel up-regulations of fatty acid translocase/CD36 (FAT/CD36) and heart fatty acid binding protein (H-FABP), while refeeding promotes down-regulation of both genes. To directly access the role of PPARδ in muscle cells, we forced its expression and that of a dominant-negative PPARδ mutant in C2C12 myogenic cells. Differentiated C2C12 cells responds to 2-bromopalmitate or synthetic PPARδ agonist by induction of genes involved in lipid metabolism and increment of fatty acid oxidation. Overexpression of PPARδ enhanced these cellular responses, whereas expression of the dominant-negative mutant exerts opposite effects. These data strongly support a role for PPARδ in the regulation of fatty acid oxidation in skeletal muscle and in adaptive response of this tissue to lipid catabolism.</description><subject>Animals</subject><subject>Biochemistry, Molecular Biology</subject><subject>Carbon Radioisotopes</subject><subject>Cell Differentiation</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Line</subject><subject>Fatty acid</subject><subject>Fatty acid oxidation</subject><subject>Fatty Acids</subject><subject>Fatty Acids - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - physiology</subject><subject>Kinetics</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscle, Skeletal</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Mutation</subject><subject>Myotube</subject><subject>Nutritional Physiological Phenomena</subject><subject>Palmitates</subject><subject>Palmitates - pharmacology</subject><subject>Receptors, Cytoplasmic and Nuclear</subject><subject>Receptors, Cytoplasmic and Nuclear - agonists</subject><subject>Receptors, Cytoplasmic and Nuclear - genetics</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>RNA, Messenger</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Transcription Factors</subject><subject>Transcription Factors - agonists</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transcriptional Activation</subject><issn>1388-1981</issn><issn>0006-3002</issn><issn>0167-4889</issn><issn>1879-2618</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcGOFCEQhonRuOvqI2g4GU1shYZu4LTZbNQ1mehBPZNqulpRuhmBnriJj-Vz-EwyO6MePUFVfVV_qn5CHnL2nDPev3jPhdYNN5o_YeIpY0zxRt4ip1wr07Q917fr_w9yQu7l_IUx3gnR3SUnvNWy5Uaekh9v15J88XGBQBN-WgPsAwrLSFMMSONEt5jid5_jjHRbc37CBCWmBlzxOyhYSXS4rSn66yf1C52glGsKzo_UQYGh9uR5X8hfMWCpSvOaXcD75M4EIeOD43tGPr56-eHyqtm8e_3m8mLTOGF0aRRz2A7Yu7GT0KpuVKDZCK2To9KsN6KWjDa6R9FJ3spOoTLIa9AObqgrn5Fnh7mfIdht8jOkaxvB26uLjfVLxjRbxoQ2Ruodr_jjA163_bZiLnb22WEIsGBcs1VCCiaVqWB3AF2KOSec_g7nzO5dsjcu2b0Flgl745KVte_RUWAdZhz_dR1tqcD5AcB6lZ3HZLPzuDgcfT11sWP0_5H4DZE9pBo</recordid><startdate>20030704</startdate><enddate>20030704</enddate><creator>Holst, Dorte</creator><creator>Luquet, Serge</creator><creator>Nogueira, Véronique</creator><creator>Kristiansen, Karsten</creator><creator>Leverve, Xavier</creator><creator>Grimaldi, Paul A.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-6024-0917</orcidid><orcidid>https://orcid.org/0000-0001-8668-6645</orcidid></search><sort><creationdate>20030704</creationdate><title>Nutritional regulation and role of peroxisome proliferator-activated receptor δ in fatty acid catabolism in skeletal muscle</title><author>Holst, Dorte ; Luquet, Serge ; Nogueira, Véronique ; Kristiansen, Karsten ; Leverve, Xavier ; Grimaldi, Paul A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-70ce2be6cd54a275d7a80da2c4d780693e6c98986e35412457e79e13542bcb533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biochemistry, Molecular Biology</topic><topic>Carbon Radioisotopes</topic><topic>Cell Differentiation</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Line</topic><topic>Fatty acid</topic><topic>Fatty acid oxidation</topic><topic>Fatty Acids</topic><topic>Fatty Acids - metabolism</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - physiology</topic><topic>Kinetics</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Muscle, Skeletal</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Mutation</topic><topic>Myotube</topic><topic>Nutritional Physiological Phenomena</topic><topic>Palmitates</topic><topic>Palmitates - pharmacology</topic><topic>Receptors, Cytoplasmic and Nuclear</topic><topic>Receptors, Cytoplasmic and Nuclear - agonists</topic><topic>Receptors, Cytoplasmic and Nuclear - genetics</topic><topic>Receptors, Cytoplasmic and Nuclear - metabolism</topic><topic>RNA, Messenger</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Transcription Factors</topic><topic>Transcription Factors - agonists</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transcriptional Activation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Holst, Dorte</creatorcontrib><creatorcontrib>Luquet, Serge</creatorcontrib><creatorcontrib>Nogueira, Véronique</creatorcontrib><creatorcontrib>Kristiansen, Karsten</creatorcontrib><creatorcontrib>Leverve, Xavier</creatorcontrib><creatorcontrib>Grimaldi, Paul A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Biochimica et biophysica acta</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Holst, Dorte</au><au>Luquet, Serge</au><au>Nogueira, Véronique</au><au>Kristiansen, Karsten</au><au>Leverve, Xavier</au><au>Grimaldi, Paul A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nutritional regulation and role of peroxisome proliferator-activated receptor δ in fatty acid catabolism in skeletal muscle</atitle><jtitle>Biochimica et biophysica acta</jtitle><addtitle>Biochim Biophys Acta</addtitle><date>2003-07-04</date><risdate>2003</risdate><volume>1633</volume><issue>1</issue><spage>43</spage><epage>50</epage><pages>43-50</pages><issn>1388-1981</issn><issn>0006-3002</issn><issn>0167-4889</issn><eissn>1879-2618</eissn><abstract>Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors primarily involved in lipid homeostasis. PPARδ displays strong expression in tissues with high lipid metabolism, such as adipose, intestine and muscle. Its role in skeletal muscle remains largely unknown. After a 24-h starvation period, PPARδ mRNA levels are dramatically up-regulated in gastrocnemius muscle of mice and restored to control level upon refeeding. The rise of PPARδ is accompanied by parallel up-regulations of fatty acid translocase/CD36 (FAT/CD36) and heart fatty acid binding protein (H-FABP), while refeeding promotes down-regulation of both genes. To directly access the role of PPARδ in muscle cells, we forced its expression and that of a dominant-negative PPARδ mutant in C2C12 myogenic cells. Differentiated C2C12 cells responds to 2-bromopalmitate or synthetic PPARδ agonist by induction of genes involved in lipid metabolism and increment of fatty acid oxidation. Overexpression of PPARδ enhanced these cellular responses, whereas expression of the dominant-negative mutant exerts opposite effects. 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| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Biochemistry, Molecular Biology Carbon Radioisotopes Cell Differentiation Cell Differentiation - drug effects Cell Line Fatty acid Fatty acid oxidation Fatty Acids Fatty Acids - metabolism Gene expression Gene Expression Regulation Gene Expression Regulation - drug effects Gene Expression Regulation - physiology Kinetics Life Sciences Male Mice Mice, Inbred C57BL Muscle, Skeletal Muscle, Skeletal - metabolism Mutation Myotube Nutritional Physiological Phenomena Palmitates Palmitates - pharmacology Receptors, Cytoplasmic and Nuclear Receptors, Cytoplasmic and Nuclear - agonists Receptors, Cytoplasmic and Nuclear - genetics Receptors, Cytoplasmic and Nuclear - metabolism RNA, Messenger RNA, Messenger - genetics RNA, Messenger - metabolism Transcription Factors Transcription Factors - agonists Transcription Factors - genetics Transcription Factors - metabolism Transcriptional Activation |
| title | Nutritional regulation and role of peroxisome proliferator-activated receptor δ in fatty acid catabolism in skeletal muscle |
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