Life without white fat: a transgenic mouse
We have generated a transgenic mouse with no white fat tissue throughout life. These mice express a dominant-negative protein, termed A-ZIP/F, under the control of the adipose-specific aP2 enhancer/promoter. This protein prevents the DNA binding of B-ZIP transcription factors of both the C/EBP and J...
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| Veröffentlicht in: | Genes & development 1998-10, Vol.12 (20), p.3168-3181 |
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| creator | Moitra, J Mason, M M Olive, M Krylov, D Gavrilova, O Marcus-Samuels, B Feigenbaum, L Lee, E Aoyama, T Eckhaus, M Reitman, M L Vinson, C |
| description | We have generated a transgenic mouse with no white fat tissue throughout life. These mice express a dominant-negative protein, termed A-ZIP/F, under the control of the adipose-specific aP2 enhancer/promoter. This protein prevents the DNA binding of B-ZIP transcription factors of both the C/EBP and Jun families. The transgenic mice (named A-ZIP/F-1) have no white adipose tissue and dramatically reduced amounts of brown adipose tissue, which is inactive. They are initially growth delayed, but by week 12, surpass their littermates in weight. The mice eat, drink, and urinate copiously, have decreased fecundity, premature death, and frequently die after anesthesia. The physiological consequences of having no white fat tissue are profound. The liver is engorged with lipid, and the internal organs are enlarged. The mice are diabetic, with reduced leptin (20-fold) and elevated serum glucose (3-fold), insulin (50- to 400-fold), free fatty acids (2-fold), and triglycerides (3- to 5-fold). The A-ZIP/F-1 phenotype suggests a mouse model for the human disease lipoatrophic diabetes (Seip-Berardinelli syndrome), indicating that the lack of fat can cause diabetes. The myriad of consequences of having no fat throughout development can be addressed with this model. |
| doi_str_mv | 10.1101/gad.12.20.3168 |
| format | Article |
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These mice express a dominant-negative protein, termed A-ZIP/F, under the control of the adipose-specific aP2 enhancer/promoter. This protein prevents the DNA binding of B-ZIP transcription factors of both the C/EBP and Jun families. The transgenic mice (named A-ZIP/F-1) have no white adipose tissue and dramatically reduced amounts of brown adipose tissue, which is inactive. They are initially growth delayed, but by week 12, surpass their littermates in weight. The mice eat, drink, and urinate copiously, have decreased fecundity, premature death, and frequently die after anesthesia. The physiological consequences of having no white fat tissue are profound. The liver is engorged with lipid, and the internal organs are enlarged. The mice are diabetic, with reduced leptin (20-fold) and elevated serum glucose (3-fold), insulin (50- to 400-fold), free fatty acids (2-fold), and triglycerides (3- to 5-fold). The A-ZIP/F-1 phenotype suggests a mouse model for the human disease lipoatrophic diabetes (Seip-Berardinelli syndrome), indicating that the lack of fat can cause diabetes. The myriad of consequences of having no fat throughout development can be addressed with this model.</description><identifier>ISSN: 0890-9369</identifier><identifier>EISSN: 1549-5477</identifier><identifier>DOI: 10.1101/gad.12.20.3168</identifier><identifier>PMID: 9784492</identifier><language>eng</language><publisher>United States: Cold Spring Harbor Laboratory Press</publisher><subject>Adipose Tissue - abnormalities ; Adipose Tissue, Brown - pathology ; Amino Acid Sequence ; Animals ; CCAAT-Enhancer-Binding Proteins ; Diabetes Mellitus, Experimental - genetics ; Diabetes Mellitus, Experimental - mortality ; Diabetes Mellitus, Experimental - pathology ; DNA-Binding Proteins - antagonists & inhibitors ; DNA-Binding Proteins - metabolism ; Fasting ; Female ; Leptin ; Leucine Zippers - genetics ; Male ; Mice ; Mice, Transgenic - genetics ; Mice, Transgenic - growth & development ; Mice, Transgenic - metabolism ; Molecular Sequence Data ; Nuclear Proteins - antagonists & inhibitors ; Nuclear Proteins - metabolism ; Phenotype ; Proteins - genetics ; Research Paper ; RNA, Messenger - biosynthesis ; Transcription Factor AP-1 - antagonists & inhibitors ; Transcription Factor AP-1 - metabolism ; Viscera - pathology</subject><ispartof>Genes & development, 1998-10, Vol.12 (20), p.3168-3181</ispartof><rights>Copyright © 1998, Cold Spring Harbor Laboratory Press 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-a55f7ef5baf864164ee5664fd663076fa611252f82d06657ef989236cf3ec70b3</citedby><cites>FETCH-LOGICAL-c481t-a55f7ef5baf864164ee5664fd663076fa611252f82d06657ef989236cf3ec70b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC317213/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC317213/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9784492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moitra, J</creatorcontrib><creatorcontrib>Mason, M M</creatorcontrib><creatorcontrib>Olive, M</creatorcontrib><creatorcontrib>Krylov, D</creatorcontrib><creatorcontrib>Gavrilova, O</creatorcontrib><creatorcontrib>Marcus-Samuels, B</creatorcontrib><creatorcontrib>Feigenbaum, L</creatorcontrib><creatorcontrib>Lee, E</creatorcontrib><creatorcontrib>Aoyama, T</creatorcontrib><creatorcontrib>Eckhaus, M</creatorcontrib><creatorcontrib>Reitman, M L</creatorcontrib><creatorcontrib>Vinson, C</creatorcontrib><title>Life without white fat: a transgenic mouse</title><title>Genes & development</title><addtitle>Genes Dev</addtitle><description>We have generated a transgenic mouse with no white fat tissue throughout life. These mice express a dominant-negative protein, termed A-ZIP/F, under the control of the adipose-specific aP2 enhancer/promoter. This protein prevents the DNA binding of B-ZIP transcription factors of both the C/EBP and Jun families. The transgenic mice (named A-ZIP/F-1) have no white adipose tissue and dramatically reduced amounts of brown adipose tissue, which is inactive. They are initially growth delayed, but by week 12, surpass their littermates in weight. The mice eat, drink, and urinate copiously, have decreased fecundity, premature death, and frequently die after anesthesia. The physiological consequences of having no white fat tissue are profound. The liver is engorged with lipid, and the internal organs are enlarged. The mice are diabetic, with reduced leptin (20-fold) and elevated serum glucose (3-fold), insulin (50- to 400-fold), free fatty acids (2-fold), and triglycerides (3- to 5-fold). The A-ZIP/F-1 phenotype suggests a mouse model for the human disease lipoatrophic diabetes (Seip-Berardinelli syndrome), indicating that the lack of fat can cause diabetes. The myriad of consequences of having no fat throughout development can be addressed with this model.</description><subject>Adipose Tissue - abnormalities</subject><subject>Adipose Tissue, Brown - pathology</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>CCAAT-Enhancer-Binding Proteins</subject><subject>Diabetes Mellitus, Experimental - genetics</subject><subject>Diabetes Mellitus, Experimental - mortality</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>DNA-Binding Proteins - antagonists & inhibitors</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Fasting</subject><subject>Female</subject><subject>Leptin</subject><subject>Leucine Zippers - genetics</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Transgenic - genetics</subject><subject>Mice, Transgenic - growth & development</subject><subject>Mice, Transgenic - metabolism</subject><subject>Molecular Sequence Data</subject><subject>Nuclear Proteins - antagonists & inhibitors</subject><subject>Nuclear Proteins - metabolism</subject><subject>Phenotype</subject><subject>Proteins - genetics</subject><subject>Research Paper</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Transcription Factor AP-1 - antagonists & inhibitors</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Viscera - pathology</subject><issn>0890-9369</issn><issn>1549-5477</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctLAzEQxoMotVav3oQ9eRB2zeQx2QgepPiCghc9h3Q3aVf2oZutxf_elJaiJ-cyh_l9wzfzEXIONAOgcL2wZQYsYzTjgPkBGYMUOpVCqUMyprmmqeaoj8lJCO-UUqSIIzLSKhdCszG5mlXeJetqWHarIVkvq8El3g43iU2G3rZh4dqqSJpuFdwpOfK2Du5s1yfk7eH-dfqUzl4en6d3s7QQOQypldIr5-Xc-hwFoHBOIgpfInKq0FsEYJL5nJXRi4yozjXjWHjuCkXnfEJut3s_VvPGlYVro5PafPRVY_tv09nK_J201dIsui_DQTHgUX-50_fd58qFwTRVKFxd29bFOwzqWMjUvyAoECL-LILZFiz6LoTe-b0ZoGaTgokpGGCGUbNJIQoufp-wx3dv5z_tVIKU</recordid><startdate>19981015</startdate><enddate>19981015</enddate><creator>Moitra, J</creator><creator>Mason, M M</creator><creator>Olive, M</creator><creator>Krylov, D</creator><creator>Gavrilova, O</creator><creator>Marcus-Samuels, B</creator><creator>Feigenbaum, L</creator><creator>Lee, E</creator><creator>Aoyama, T</creator><creator>Eckhaus, M</creator><creator>Reitman, M L</creator><creator>Vinson, C</creator><general>Cold Spring Harbor Laboratory Press</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19981015</creationdate><title>Life without white fat: a transgenic mouse</title><author>Moitra, J ; Mason, M M ; Olive, M ; Krylov, D ; Gavrilova, O ; Marcus-Samuels, B ; Feigenbaum, L ; Lee, E ; Aoyama, T ; Eckhaus, M ; Reitman, M L ; Vinson, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-a55f7ef5baf864164ee5664fd663076fa611252f82d06657ef989236cf3ec70b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adipose Tissue - abnormalities</topic><topic>Adipose Tissue, Brown - pathology</topic><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>CCAAT-Enhancer-Binding Proteins</topic><topic>Diabetes Mellitus, Experimental - genetics</topic><topic>Diabetes Mellitus, Experimental - mortality</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>DNA-Binding Proteins - antagonists & inhibitors</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Fasting</topic><topic>Female</topic><topic>Leptin</topic><topic>Leucine Zippers - genetics</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Transgenic - genetics</topic><topic>Mice, Transgenic - growth & development</topic><topic>Mice, Transgenic - metabolism</topic><topic>Molecular Sequence Data</topic><topic>Nuclear Proteins - antagonists & inhibitors</topic><topic>Nuclear Proteins - metabolism</topic><topic>Phenotype</topic><topic>Proteins - genetics</topic><topic>Research Paper</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Transcription Factor AP-1 - antagonists & inhibitors</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Viscera - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moitra, J</creatorcontrib><creatorcontrib>Mason, M M</creatorcontrib><creatorcontrib>Olive, M</creatorcontrib><creatorcontrib>Krylov, D</creatorcontrib><creatorcontrib>Gavrilova, O</creatorcontrib><creatorcontrib>Marcus-Samuels, B</creatorcontrib><creatorcontrib>Feigenbaum, L</creatorcontrib><creatorcontrib>Lee, E</creatorcontrib><creatorcontrib>Aoyama, T</creatorcontrib><creatorcontrib>Eckhaus, M</creatorcontrib><creatorcontrib>Reitman, M L</creatorcontrib><creatorcontrib>Vinson, C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes & development</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moitra, J</au><au>Mason, M M</au><au>Olive, M</au><au>Krylov, D</au><au>Gavrilova, O</au><au>Marcus-Samuels, B</au><au>Feigenbaum, L</au><au>Lee, E</au><au>Aoyama, T</au><au>Eckhaus, M</au><au>Reitman, M L</au><au>Vinson, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Life without white fat: a transgenic mouse</atitle><jtitle>Genes & development</jtitle><addtitle>Genes Dev</addtitle><date>1998-10-15</date><risdate>1998</risdate><volume>12</volume><issue>20</issue><spage>3168</spage><epage>3181</epage><pages>3168-3181</pages><issn>0890-9369</issn><eissn>1549-5477</eissn><abstract>We have generated a transgenic mouse with no white fat tissue throughout life. These mice express a dominant-negative protein, termed A-ZIP/F, under the control of the adipose-specific aP2 enhancer/promoter. This protein prevents the DNA binding of B-ZIP transcription factors of both the C/EBP and Jun families. The transgenic mice (named A-ZIP/F-1) have no white adipose tissue and dramatically reduced amounts of brown adipose tissue, which is inactive. They are initially growth delayed, but by week 12, surpass their littermates in weight. The mice eat, drink, and urinate copiously, have decreased fecundity, premature death, and frequently die after anesthesia. The physiological consequences of having no white fat tissue are profound. The liver is engorged with lipid, and the internal organs are enlarged. The mice are diabetic, with reduced leptin (20-fold) and elevated serum glucose (3-fold), insulin (50- to 400-fold), free fatty acids (2-fold), and triglycerides (3- to 5-fold). The A-ZIP/F-1 phenotype suggests a mouse model for the human disease lipoatrophic diabetes (Seip-Berardinelli syndrome), indicating that the lack of fat can cause diabetes. The myriad of consequences of having no fat throughout development can be addressed with this model.</abstract><cop>United States</cop><pub>Cold Spring Harbor Laboratory Press</pub><pmid>9784492</pmid><doi>10.1101/gad.12.20.3168</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adipose Tissue - abnormalities Adipose Tissue, Brown - pathology Amino Acid Sequence Animals CCAAT-Enhancer-Binding Proteins Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - mortality Diabetes Mellitus, Experimental - pathology DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - metabolism Fasting Female Leptin Leucine Zippers - genetics Male Mice Mice, Transgenic - genetics Mice, Transgenic - growth & development Mice, Transgenic - metabolism Molecular Sequence Data Nuclear Proteins - antagonists & inhibitors Nuclear Proteins - metabolism Phenotype Proteins - genetics Research Paper RNA, Messenger - biosynthesis Transcription Factor AP-1 - antagonists & inhibitors Transcription Factor AP-1 - metabolism Viscera - pathology |
| title | Life without white fat: a transgenic mouse |
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