Ligand- and species-dependent activation of PPARalpha
Peroxisome proliferator-activated receptor alpha (PPARalpha) is mainly expressed in liver and involved in lipid metabolism. Oxidation of certain fatty acids in peroxisomes is under PPARalpha control. A wide variety of lipid molecules activate PPARalpha as well as the fibric acid derivative clofibrat...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2004, Vol.14 (4-6), p.269-276 |
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| container_title | Cellular physiology and biochemistry |
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| creator | Akbiyik, Filiz Ray, Denise M Bozkaya, Hakan Demirpence, Ediz |
| description | Peroxisome proliferator-activated receptor alpha (PPARalpha) is mainly expressed in liver and involved in lipid metabolism. Oxidation of certain fatty acids in peroxisomes is under PPARalpha control. A wide variety of lipid molecules activate PPARalpha as well as the fibric acid derivative clofibrate. In the present study, we evaluated the differential activation of PPARalpha with several agonist ligands through its expression and DNA binding in both rat (McA-RH7777) and human (HepG2) hepatoma cell lines. In McA-RH7777 cells, clofibrate alone mediated a higher induction of PPARalpha expression than linoleic acid. In contrast, linoleic acid was the most effective ligand in HepG2 cells and treatment with clofibrate plus linoleic acid did not further increase PPARalpha expression. PPRE-binding activity of PPARalpha in ligand-treated cells was also increased in a parallel manner. We suggest that ligand-induced PPARalpha activation might give rise to differential species-dependent responses. |
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Oxidation of certain fatty acids in peroxisomes is under PPARalpha control. A wide variety of lipid molecules activate PPARalpha as well as the fibric acid derivative clofibrate. In the present study, we evaluated the differential activation of PPARalpha with several agonist ligands through its expression and DNA binding in both rat (McA-RH7777) and human (HepG2) hepatoma cell lines. In McA-RH7777 cells, clofibrate alone mediated a higher induction of PPARalpha expression than linoleic acid. In contrast, linoleic acid was the most effective ligand in HepG2 cells and treatment with clofibrate plus linoleic acid did not further increase PPARalpha expression. PPRE-binding activity of PPARalpha in ligand-treated cells was also increased in a parallel manner. We suggest that ligand-induced PPARalpha activation might give rise to differential species-dependent responses.</description><identifier>ISSN: 1015-8987</identifier><identifier>PMID: 15319530</identifier><language>eng</language><publisher>Germany</publisher><subject>Animals ; Carcinoma, Hepatocellular - metabolism ; Cell Line, Tumor ; Cell Survival ; Clofibrate - pharmacology ; DNA - metabolism ; Electrophoretic Mobility Shift Assay ; Fatty Acids, Unsaturated - metabolism ; Fatty Acids, Unsaturated - pharmacology ; Fatty Acids, Unsaturated - physiology ; Humans ; Ligands ; Linoleic Acid - pharmacology ; Linoleic Acid - physiology ; Liver - metabolism ; PPAR alpha - agonists ; PPAR alpha - analysis ; PPAR alpha - physiology ; Rats ; Species Specificity</subject><ispartof>Cellular physiology and biochemistry, 2004, Vol.14 (4-6), p.269-276</ispartof><rights>Copyright 2004 S. 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We suggest that ligand-induced PPARalpha activation might give rise to differential species-dependent responses.</description><subject>Animals</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival</subject><subject>Clofibrate - pharmacology</subject><subject>DNA - metabolism</subject><subject>Electrophoretic Mobility Shift Assay</subject><subject>Fatty Acids, Unsaturated - metabolism</subject><subject>Fatty Acids, Unsaturated - pharmacology</subject><subject>Fatty Acids, Unsaturated - physiology</subject><subject>Humans</subject><subject>Ligands</subject><subject>Linoleic Acid - pharmacology</subject><subject>Linoleic Acid - physiology</subject><subject>Liver - metabolism</subject><subject>PPAR alpha - agonists</subject><subject>PPAR alpha - analysis</subject><subject>PPAR alpha - physiology</subject><subject>Rats</subject><subject>Species Specificity</subject><issn>1015-8987</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1j0tLxDAUhbNQnHH0L0hX7gJ5N10Ogy8oOKj7cpvcaKSP2LSC_96C4-Z8HPg4cM7IljOuqa1suSGXOX-ytZaVuCAbriWvtGRbouv4DoOnxRpFTugiZuox4eBxmAtwc_yGOY5DMYbieNy_QJc-4IqcB-gyXp-4I6_3d2-HR1o_Pzwd9jVNWjEqXOmCLFUVvPeqtJIraAX3AdAybiUwG4Q3rjVOWWMEBnQBlNEsMAZW7sjt32qaxq8F89z0MTvsOhhwXHJjjGWaSb2KNydxaXv0TZpiD9NP839T_gKXWEyu</recordid><startdate>2004</startdate><enddate>2004</enddate><creator>Akbiyik, Filiz</creator><creator>Ray, Denise M</creator><creator>Bozkaya, Hakan</creator><creator>Demirpence, Ediz</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>2004</creationdate><title>Ligand- and species-dependent activation of PPARalpha</title><author>Akbiyik, Filiz ; Ray, Denise M ; Bozkaya, Hakan ; Demirpence, Ediz</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p540-2c7cf3749fddd478314ab21dfae80183a08f2d6cb6c48662efecfa4650f00a83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival</topic><topic>Clofibrate - pharmacology</topic><topic>DNA - metabolism</topic><topic>Electrophoretic Mobility Shift Assay</topic><topic>Fatty Acids, Unsaturated - metabolism</topic><topic>Fatty Acids, Unsaturated - pharmacology</topic><topic>Fatty Acids, Unsaturated - physiology</topic><topic>Humans</topic><topic>Ligands</topic><topic>Linoleic Acid - pharmacology</topic><topic>Linoleic Acid - physiology</topic><topic>Liver - metabolism</topic><topic>PPAR alpha - agonists</topic><topic>PPAR alpha - analysis</topic><topic>PPAR alpha - physiology</topic><topic>Rats</topic><topic>Species Specificity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Akbiyik, Filiz</creatorcontrib><creatorcontrib>Ray, Denise M</creatorcontrib><creatorcontrib>Bozkaya, Hakan</creatorcontrib><creatorcontrib>Demirpence, Ediz</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Akbiyik, Filiz</au><au>Ray, Denise M</au><au>Bozkaya, Hakan</au><au>Demirpence, Ediz</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ligand- and species-dependent activation of PPARalpha</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2004</date><risdate>2004</risdate><volume>14</volume><issue>4-6</issue><spage>269</spage><epage>276</epage><pages>269-276</pages><issn>1015-8987</issn><abstract>Peroxisome proliferator-activated receptor alpha (PPARalpha) is mainly expressed in liver and involved in lipid metabolism. 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| ispartof | Cellular physiology and biochemistry, 2004, Vol.14 (4-6), p.269-276 |
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| language | eng |
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| source | MEDLINE; Karger Journals |
| subjects | Animals Carcinoma, Hepatocellular - metabolism Cell Line, Tumor Cell Survival Clofibrate - pharmacology DNA - metabolism Electrophoretic Mobility Shift Assay Fatty Acids, Unsaturated - metabolism Fatty Acids, Unsaturated - pharmacology Fatty Acids, Unsaturated - physiology Humans Ligands Linoleic Acid - pharmacology Linoleic Acid - physiology Liver - metabolism PPAR alpha - agonists PPAR alpha - analysis PPAR alpha - physiology Rats Species Specificity |
| title | Ligand- and species-dependent activation of PPARalpha |
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