Bile acid represses the peroxisome proliferator-activated receptor-γ coactivator-1 promoter activity in a small heterodimer partner-dependent manner
Bile acid homeostasis is tightly controlled by the feedback mechanism in which an atypical orphan nuclear receptor (NR), small heterodimer partner (SHP), inactivates several transcription factors. We previously demonstrated that bile acid represses the expression of gluconeogenic genes, including gl...
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| Veröffentlicht in: | International journal of molecular medicine 2007-05, Vol.19 (5), p.751-756 |
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| container_title | International journal of molecular medicine |
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| creator | Yamagata, Kazuyuki Yoshimochi, Kenji Daitoku, Hiroaki Hirota, Keiko Fukamizu, Akiyoshi |
| description | Bile acid homeostasis is tightly controlled by the feedback mechanism in
which an atypical orphan nuclear receptor (NR), small heterodimer partner (SHP),
inactivates several transcription factors. We previously demonstrated that bile
acid represses the expression of gluconeogenic genes, including glucose-6-phosphatase
(G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), and fructose-1,6-bisphosphatase
(FBP1) in an SHP-dependent manner. Recently, peroxisome proliferator-activated
receptor-γ (PPAR-γ) coactivator-1 (PGC-1) gene, a coactivator of NRs important
for gluconeogenic gene expression, was also downregulated by bile acid in wild-type
mice but not in farnesoid X receptor- or SHP-null mice. However, the molecular
mechanism for the effect of bile acid on PGC-1 gene expression remains unknown.
In the present study, a series of reporter assays demonstrated that the promoter
activity of PGC-1 via a member of the forkhead transcription factors, Foxo1, FOXO3a,
and Foxo4 was downregulated by treatment with chenodeoxicholic acid and with transfected
SHP. These results revealed that bile acid inhibits the promoter activity of PGC-1
in an SHP-dependent manner. |
| doi_str_mv | 10.3892/ijmm.19.5.751 |
| format | Article |
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which an atypical orphan nuclear receptor (NR), small heterodimer partner (SHP),
inactivates several transcription factors. We previously demonstrated that bile
acid represses the expression of gluconeogenic genes, including glucose-6-phosphatase
(G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), and fructose-1,6-bisphosphatase
(FBP1) in an SHP-dependent manner. Recently, peroxisome proliferator-activated
receptor-γ (PPAR-γ) coactivator-1 (PGC-1) gene, a coactivator of NRs important
for gluconeogenic gene expression, was also downregulated by bile acid in wild-type
mice but not in farnesoid X receptor- or SHP-null mice. However, the molecular
mechanism for the effect of bile acid on PGC-1 gene expression remains unknown.
In the present study, a series of reporter assays demonstrated that the promoter
activity of PGC-1 via a member of the forkhead transcription factors, Foxo1, FOXO3a,
and Foxo4 was downregulated by treatment with chenodeoxicholic acid and with transfected
SHP. These results revealed that bile acid inhibits the promoter activity of PGC-1
in an SHP-dependent manner.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.19.5.751</identifier><identifier>PMID: 17390079</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Animals ; Bile Acids and Salts - pharmacology ; Down-Regulation - drug effects ; Forkhead Box Protein O1 ; Forkhead Transcription Factors - metabolism ; Gluconeogenesis - drug effects ; Gluconeogenesis - genetics ; Humans ; Mice ; Models, Genetic ; Promoter Regions, Genetic - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Receptors, Cytoplasmic and Nuclear - metabolism ; Transcription Factors - genetics</subject><ispartof>International journal of molecular medicine, 2007-05, Vol.19 (5), p.751-756</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c366t-d81fe83296ddf2322346698fed9998b15a3babc9f1f1a30d32bf4cb3168a2f903</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17390079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamagata, Kazuyuki</creatorcontrib><creatorcontrib>Yoshimochi, Kenji</creatorcontrib><creatorcontrib>Daitoku, Hiroaki</creatorcontrib><creatorcontrib>Hirota, Keiko</creatorcontrib><creatorcontrib>Fukamizu, Akiyoshi</creatorcontrib><title>Bile acid represses the peroxisome proliferator-activated receptor-γ coactivator-1 promoter activity in a small heterodimer partner-dependent manner</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Bile acid homeostasis is tightly controlled by the feedback mechanism in
which an atypical orphan nuclear receptor (NR), small heterodimer partner (SHP),
inactivates several transcription factors. We previously demonstrated that bile
acid represses the expression of gluconeogenic genes, including glucose-6-phosphatase
(G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), and fructose-1,6-bisphosphatase
(FBP1) in an SHP-dependent manner. Recently, peroxisome proliferator-activated
receptor-γ (PPAR-γ) coactivator-1 (PGC-1) gene, a coactivator of NRs important
for gluconeogenic gene expression, was also downregulated by bile acid in wild-type
mice but not in farnesoid X receptor- or SHP-null mice. However, the molecular
mechanism for the effect of bile acid on PGC-1 gene expression remains unknown.
In the present study, a series of reporter assays demonstrated that the promoter
activity of PGC-1 via a member of the forkhead transcription factors, Foxo1, FOXO3a,
and Foxo4 was downregulated by treatment with chenodeoxicholic acid and with transfected
SHP. These results revealed that bile acid inhibits the promoter activity of PGC-1
in an SHP-dependent manner.</description><subject>Animals</subject><subject>Bile Acids and Salts - pharmacology</subject><subject>Down-Regulation - drug effects</subject><subject>Forkhead Box Protein O1</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gluconeogenesis - drug effects</subject><subject>Gluconeogenesis - genetics</subject><subject>Humans</subject><subject>Mice</subject><subject>Models, Genetic</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>Transcription Factors - genetics</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkc9OHSEYxUljU6122W3Dyo2ZK39mmGGpptYmJt20iTvCwEfEDMMIXFMfxCfpe_SZyvRe44rD-X6cfOEg9JmSDR8kO_cPIWyo3HSbvqPv0BHtJW1Y294dVE1J3_C-E4foY84PhLCulcMHdEh7Lgnp5RF6ufQTYG28xQmWBDlDxuUe8AIp_vY5hipTnLyDpEtMjTbFP-kCK29gWa2_f7CJe79e6fogxAIJ_zd9ecZ-xhrnoKcJ30OdROtDnS86lRlSY2GB2cJccNBzNU7Qe6enDJ_25zH6df3159VNc_vj2_eri9vGcCFKYwfqYOBMCmsd44zxVgg5OLBSymGkneajHo101FHNieVsdK0ZORWDZk4SfoxOd7l148ct5KKCzwamSc8Qt1n1hBMhO1HBZgeaFHNO4NSSfNDpWVGi1h7U2oOiUnWq9lD5L_vg7RjAvtH7j6_A2Q7Ii56ttzG_Ma-tUdnVrCr4P6o_lwo</recordid><startdate>20070501</startdate><enddate>20070501</enddate><creator>Yamagata, Kazuyuki</creator><creator>Yoshimochi, Kenji</creator><creator>Daitoku, Hiroaki</creator><creator>Hirota, Keiko</creator><creator>Fukamizu, Akiyoshi</creator><general>D.A. Spandidos</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></search><sort><creationdate>20070501</creationdate><title>Bile acid represses the peroxisome proliferator-activated receptor-γ coactivator-1 promoter activity in a small heterodimer partner-dependent manner</title><author>Yamagata, Kazuyuki ; Yoshimochi, Kenji ; Daitoku, Hiroaki ; Hirota, Keiko ; Fukamizu, Akiyoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c366t-d81fe83296ddf2322346698fed9998b15a3babc9f1f1a30d32bf4cb3168a2f903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Bile Acids and Salts - pharmacology</topic><topic>Down-Regulation - drug effects</topic><topic>Forkhead Box Protein O1</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gluconeogenesis - drug effects</topic><topic>Gluconeogenesis - genetics</topic><topic>Humans</topic><topic>Mice</topic><topic>Models, Genetic</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Receptors, Cytoplasmic and Nuclear - metabolism</topic><topic>Transcription Factors - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamagata, Kazuyuki</creatorcontrib><creatorcontrib>Yoshimochi, Kenji</creatorcontrib><creatorcontrib>Daitoku, Hiroaki</creatorcontrib><creatorcontrib>Hirota, Keiko</creatorcontrib><creatorcontrib>Fukamizu, Akiyoshi</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><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamagata, Kazuyuki</au><au>Yoshimochi, Kenji</au><au>Daitoku, Hiroaki</au><au>Hirota, Keiko</au><au>Fukamizu, Akiyoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bile acid represses the peroxisome proliferator-activated receptor-γ coactivator-1 promoter activity in a small heterodimer partner-dependent manner</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2007-05-01</date><risdate>2007</risdate><volume>19</volume><issue>5</issue><spage>751</spage><epage>756</epage><pages>751-756</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>Bile acid homeostasis is tightly controlled by the feedback mechanism in
which an atypical orphan nuclear receptor (NR), small heterodimer partner (SHP),
inactivates several transcription factors. We previously demonstrated that bile
acid represses the expression of gluconeogenic genes, including glucose-6-phosphatase
(G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), and fructose-1,6-bisphosphatase
(FBP1) in an SHP-dependent manner. Recently, peroxisome proliferator-activated
receptor-γ (PPAR-γ) coactivator-1 (PGC-1) gene, a coactivator of NRs important
for gluconeogenic gene expression, was also downregulated by bile acid in wild-type
mice but not in farnesoid X receptor- or SHP-null mice. However, the molecular
mechanism for the effect of bile acid on PGC-1 gene expression remains unknown.
In the present study, a series of reporter assays demonstrated that the promoter
activity of PGC-1 via a member of the forkhead transcription factors, Foxo1, FOXO3a,
and Foxo4 was downregulated by treatment with chenodeoxicholic acid and with transfected
SHP. These results revealed that bile acid inhibits the promoter activity of PGC-1
in an SHP-dependent manner.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>17390079</pmid><doi>10.3892/ijmm.19.5.751</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1107-3756 1791-244X |
| language | eng |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Bile Acids and Salts - pharmacology Down-Regulation - drug effects Forkhead Box Protein O1 Forkhead Transcription Factors - metabolism Gluconeogenesis - drug effects Gluconeogenesis - genetics Humans Mice Models, Genetic Promoter Regions, Genetic - genetics Proto-Oncogene Proteins c-akt - metabolism Receptors, Cytoplasmic and Nuclear - metabolism Transcription Factors - genetics |
| title | Bile acid represses the peroxisome proliferator-activated receptor-γ coactivator-1 promoter activity in a small heterodimer partner-dependent manner |
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