Regulation of the Third Member of the Uncoupling Protein Family, UCP3, by Cold and Thyroid Hormone
Uncoupling protein (UCP1) is a transmembrane proton transporter present in the mitochondria of brown adipose tissue (BAT), a specialized tissue which functions in temperature homeostasis and energy balance (Nicholls, D. G., and Locke, R. M. (1984)Physiol. Rev.64, 2–40; Lowell, D. D., and Flier, J. S...
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| Veröffentlicht in: | Biochemical and biophysical research communications 1997-11, Vol.240 (1), p.222-227 |
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| creator | Larkin, Sarah Mull, Emily Miao, Wendy Pittner, Richard Albrandt, Keith Moore, Candace Young, Andrew Denaro, Maurizio Beaumont, Kevin |
| description | Uncoupling protein (UCP1) is a transmembrane proton transporter present in the mitochondria of brown adipose tissue (BAT), a specialized tissue which functions in temperature homeostasis and energy balance (Nicholls, D. G., and Locke, R. M. (1984)Physiol. Rev.64, 2–40; Lowell, D. D., and Flier, J. S. (1997)Annu. Rev. Med.). UCP1 mediates the thermogenesis that is characteristic of BAT by uncoupling mitochondrial oxidation of substrates from ATP synthesis. Recently, two proteins related to UCP1 have been identified and designated UCP2 (Fleury, C.,et al.(1997)Nature Genetics15, 269–272) or UCP homolog (UCPH) (Gimeno, R. E.,et al.(1997)Diabetes46, 900–906) and UCP3 (Boss, O.,et al.(1997)FEBS Lett.408, 39–42; Vidal-Puig, A.,et al.(1997)Biochem. Biophys. Res. Commun.235, 79–82). We investigated the regulation in rats of UCP3, which is expressed primarily in skeletal muscle and BAT. Expression of rat UCP3 mRNA in BAT was upregulated by in vivo treatment with triiodothyronine (T3) and by exposure to cold, suggesting that UCP3 is active in thermogenesis and energy expenditure. In skeletal muscle, UCP3 mRNA was also upregulated by T3but, surprisingly, not by cold exposure. A hypothesis is proposed to account for this differential regulation. |
| doi_str_mv | 10.1006/bbrc.1997.7636 |
| format | Article |
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G., and Locke, R. M. (1984)Physiol. Rev.64, 2–40; Lowell, D. D., and Flier, J. S. (1997)Annu. Rev. Med.). UCP1 mediates the thermogenesis that is characteristic of BAT by uncoupling mitochondrial oxidation of substrates from ATP synthesis. Recently, two proteins related to UCP1 have been identified and designated UCP2 (Fleury, C.,et al.(1997)Nature Genetics15, 269–272) or UCP homolog (UCPH) (Gimeno, R. E.,et al.(1997)Diabetes46, 900–906) and UCP3 (Boss, O.,et al.(1997)FEBS Lett.408, 39–42; Vidal-Puig, A.,et al.(1997)Biochem. Biophys. Res. Commun.235, 79–82). We investigated the regulation in rats of UCP3, which is expressed primarily in skeletal muscle and BAT. Expression of rat UCP3 mRNA in BAT was upregulated by in vivo treatment with triiodothyronine (T3) and by exposure to cold, suggesting that UCP3 is active in thermogenesis and energy expenditure. In skeletal muscle, UCP3 mRNA was also upregulated by T3but, surprisingly, not by cold exposure. A hypothesis is proposed to account for this differential regulation.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1006/bbrc.1997.7636</identifier><identifier>PMID: 9367914</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adipose Tissue, Brown - drug effects ; Adipose Tissue, Brown - metabolism ; Administration, Oral ; Animals ; Carrier Proteins - drug effects ; Carrier Proteins - metabolism ; Cloning, Molecular ; Cold Temperature ; Dietary Fats - administration & dosage ; Humans ; Ion Channels ; Male ; Mitochondria, Muscle - drug effects ; Mitochondria, Muscle - metabolism ; Mitochondrial Proteins ; Muscle, Skeletal - metabolism ; Organ Specificity - genetics ; Rats ; Rats, Inbred Strains ; RNA, Messenger - analysis ; Triiodothyronine - administration & dosage ; Triiodothyronine - pharmacology ; Uncoupling Protein 3</subject><ispartof>Biochemical and biophysical research communications, 1997-11, Vol.240 (1), p.222-227</ispartof><rights>1997 Academic Press</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-732d5b1eab2011dc2b853144bde4c30298971e281ae7e9096367ac550384e98d3</citedby><cites>FETCH-LOGICAL-c405t-732d5b1eab2011dc2b853144bde4c30298971e281ae7e9096367ac550384e98d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/bbrc.1997.7636$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9367914$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Larkin, Sarah</creatorcontrib><creatorcontrib>Mull, Emily</creatorcontrib><creatorcontrib>Miao, Wendy</creatorcontrib><creatorcontrib>Pittner, Richard</creatorcontrib><creatorcontrib>Albrandt, Keith</creatorcontrib><creatorcontrib>Moore, Candace</creatorcontrib><creatorcontrib>Young, Andrew</creatorcontrib><creatorcontrib>Denaro, Maurizio</creatorcontrib><creatorcontrib>Beaumont, Kevin</creatorcontrib><title>Regulation of the Third Member of the Uncoupling Protein Family, UCP3, by Cold and Thyroid Hormone</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Uncoupling protein (UCP1) is a transmembrane proton transporter present in the mitochondria of brown adipose tissue (BAT), a specialized tissue which functions in temperature homeostasis and energy balance (Nicholls, D. G., and Locke, R. M. (1984)Physiol. Rev.64, 2–40; Lowell, D. D., and Flier, J. S. (1997)Annu. Rev. Med.). UCP1 mediates the thermogenesis that is characteristic of BAT by uncoupling mitochondrial oxidation of substrates from ATP synthesis. Recently, two proteins related to UCP1 have been identified and designated UCP2 (Fleury, C.,et al.(1997)Nature Genetics15, 269–272) or UCP homolog (UCPH) (Gimeno, R. E.,et al.(1997)Diabetes46, 900–906) and UCP3 (Boss, O.,et al.(1997)FEBS Lett.408, 39–42; Vidal-Puig, A.,et al.(1997)Biochem. Biophys. Res. Commun.235, 79–82). We investigated the regulation in rats of UCP3, which is expressed primarily in skeletal muscle and BAT. Expression of rat UCP3 mRNA in BAT was upregulated by in vivo treatment with triiodothyronine (T3) and by exposure to cold, suggesting that UCP3 is active in thermogenesis and energy expenditure. In skeletal muscle, UCP3 mRNA was also upregulated by T3but, surprisingly, not by cold exposure. A hypothesis is proposed to account for this differential regulation.</description><subject>Adipose Tissue, Brown - drug effects</subject><subject>Adipose Tissue, Brown - metabolism</subject><subject>Administration, Oral</subject><subject>Animals</subject><subject>Carrier Proteins - drug effects</subject><subject>Carrier Proteins - metabolism</subject><subject>Cloning, Molecular</subject><subject>Cold Temperature</subject><subject>Dietary Fats - administration & dosage</subject><subject>Humans</subject><subject>Ion Channels</subject><subject>Male</subject><subject>Mitochondria, Muscle - drug effects</subject><subject>Mitochondria, Muscle - metabolism</subject><subject>Mitochondrial Proteins</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Organ Specificity - genetics</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>RNA, Messenger - analysis</subject><subject>Triiodothyronine - administration & dosage</subject><subject>Triiodothyronine - pharmacology</subject><subject>Uncoupling Protein 3</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM1LAzEQxYMotVav3oScPHVrspv9yFGKtULFIi14C_mYtpHdTU12hf3v3dLqzdPAvDePeT-EbimZUEKyB6W8nlDO80meJdkZGlLCSRRTws7RkPSOKOb04xJdhfBJCKUs4wM04EmWc8qGSL3Dti1lY12N3QY3O8CrnfUGv0KlwP_u1rV27b609RYvvWvA1ngmK1t2Y7yeLpMxVh2eutJgWZs-oPPOGjx3vnI1XKOLjSwD3JzmCK1nT6vpPFq8Pb9MHxeRZiRtojyJTaooSBX3bxodqyJNKGPKANMJiXnBcwpxQSXkwAnv2-ZSpylJCga8MMkI3R9z9959tRAaUdmgoSxlDa4NIucsLtIi642To1F7F4KHjdh7W0nfCUrEAao4QBUHqOIAtT-4OyW3qgLzZz9R7PXiqENf79uCF0FbqDUY60E3wjj7X_QPzkSEZg</recordid><startdate>19971107</startdate><enddate>19971107</enddate><creator>Larkin, Sarah</creator><creator>Mull, Emily</creator><creator>Miao, Wendy</creator><creator>Pittner, Richard</creator><creator>Albrandt, Keith</creator><creator>Moore, Candace</creator><creator>Young, Andrew</creator><creator>Denaro, Maurizio</creator><creator>Beaumont, Kevin</creator><general>Elsevier Inc</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>19971107</creationdate><title>Regulation of the Third Member of the Uncoupling Protein Family, UCP3, by Cold and Thyroid Hormone</title><author>Larkin, Sarah ; 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G., and Locke, R. M. (1984)Physiol. Rev.64, 2–40; Lowell, D. D., and Flier, J. S. (1997)Annu. Rev. Med.). UCP1 mediates the thermogenesis that is characteristic of BAT by uncoupling mitochondrial oxidation of substrates from ATP synthesis. Recently, two proteins related to UCP1 have been identified and designated UCP2 (Fleury, C.,et al.(1997)Nature Genetics15, 269–272) or UCP homolog (UCPH) (Gimeno, R. E.,et al.(1997)Diabetes46, 900–906) and UCP3 (Boss, O.,et al.(1997)FEBS Lett.408, 39–42; Vidal-Puig, A.,et al.(1997)Biochem. Biophys. Res. Commun.235, 79–82). We investigated the regulation in rats of UCP3, which is expressed primarily in skeletal muscle and BAT. Expression of rat UCP3 mRNA in BAT was upregulated by in vivo treatment with triiodothyronine (T3) and by exposure to cold, suggesting that UCP3 is active in thermogenesis and energy expenditure. In skeletal muscle, UCP3 mRNA was also upregulated by T3but, surprisingly, not by cold exposure. 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| subjects | Adipose Tissue, Brown - drug effects Adipose Tissue, Brown - metabolism Administration, Oral Animals Carrier Proteins - drug effects Carrier Proteins - metabolism Cloning, Molecular Cold Temperature Dietary Fats - administration & dosage Humans Ion Channels Male Mitochondria, Muscle - drug effects Mitochondria, Muscle - metabolism Mitochondrial Proteins Muscle, Skeletal - metabolism Organ Specificity - genetics Rats Rats, Inbred Strains RNA, Messenger - analysis Triiodothyronine - administration & dosage Triiodothyronine - pharmacology Uncoupling Protein 3 |
| title | Regulation of the Third Member of the Uncoupling Protein Family, UCP3, by Cold and Thyroid Hormone |
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