Tumor Necrosis Factor α Mediates Apoptosis of Brown Adipocytes and Defective Brown Adipocyte Function in Obesity
Severe quantitative and qualitative brown adipocyte defects are common in obesity. To investigate whether aberrant expression of tumor necrosis factor α (TNF-α ) in obesity is involved in functional brown fat atrophy, we have studied genetically obese (ob/ob) mice with targeted null mutations in the...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2000-07, Vol.97 (14), p.8033-8038 |
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| creator | Nisoli, Enzo Briscini, Luca Giordano, Antonio Tonello, Cristina Wiesbrock, Sarah M. Uysal, K. Teoman Cinti, Saverio Carruba, Michele O. Hotamisligil, Gokhan S. |
| description | Severe quantitative and qualitative brown adipocyte defects are common in obesity. To investigate whether aberrant expression of tumor necrosis factor α (TNF-α ) in obesity is involved in functional brown fat atrophy, we have studied genetically obese (ob/ob) mice with targeted null mutations in the genes encoding the two TNF receptors. The absence of both TNF receptors or p55 receptor alone resulted in a significant reduction in brown adipocyte apoptosis and an increase in β3-adrenoreceptor and uncoupling protein-1 expression in obese mice. Increased numbers of multilocular functionally active brown adipocytes, and improved thermoregulation was also observed in obese animals lacking TNF-α function. These results indicate that TNF-α plays an important role in multiple aspects of brown adipose tissue biology and mediates the abnormalities that occur at this site in obesity. |
| doi_str_mv | 10.1073/pnas.97.14.8033 |
| format | Article |
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Increased numbers of multilocular functionally active brown adipocytes, and improved thermoregulation was also observed in obese animals lacking TNF-α function. These results indicate that TNF-α plays an important role in multiple aspects of brown adipose tissue biology and mediates the abnormalities that occur at this site in obesity.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.97.14.8033</identifier><identifier>PMID: 10884431</identifier><language>eng</language><publisher>United States: National Academy of Sciences of the United States of America</publisher><subject>Adaptation, Physiological ; Adipocytes ; Adipocytes - cytology ; Adipocytes - drug effects ; Adipose Tissue, Brown - cytology ; Adipose Tissue, Brown - drug effects ; Animals ; Antigens, CD - genetics ; Apoptosis ; b3-adrenoreceptors ; Biological Sciences ; Body Temperature ; Body weight ; Brown adipocytes ; Brown adipose tissue ; Carrier Proteins - metabolism ; Cold Temperature ; Cyclic AMP - biosynthesis ; Genetics ; In Situ Nick-End Labeling ; Insulin ; Insulin resistance ; Ion Channels ; Medical research ; Membrane Proteins - metabolism ; Messenger RNA ; Mice ; Mice, Mutant Strains ; Mitochondrial Proteins ; Mutation ; Obesity ; Obesity - metabolism ; Receptors, Adrenergic, beta - metabolism ; Receptors, Adrenergic, beta-3 ; Receptors, Tumor Necrosis Factor - genetics ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tumor Necrosis Factor-alpha - pharmacology ; Uncoupling Agents - metabolism ; Uncoupling Protein 1</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2000-07, Vol.97 (14), p.8033-8038</ispartof><rights>Copyright 1993-2000 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Jul 5, 2000</rights><rights>Copyright © 2000, The National Academy of Sciences 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c520t-fd3d6241361d3de97dd35c90fbbf66821740e4064752972abf51590b7e185a5c3</citedby><cites>FETCH-LOGICAL-c520t-fd3d6241361d3de97dd35c90fbbf66821740e4064752972abf51590b7e185a5c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/97/14.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/123045$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/123045$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10884431$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nisoli, Enzo</creatorcontrib><creatorcontrib>Briscini, Luca</creatorcontrib><creatorcontrib>Giordano, Antonio</creatorcontrib><creatorcontrib>Tonello, Cristina</creatorcontrib><creatorcontrib>Wiesbrock, Sarah M.</creatorcontrib><creatorcontrib>Uysal, K. Teoman</creatorcontrib><creatorcontrib>Cinti, Saverio</creatorcontrib><creatorcontrib>Carruba, Michele O.</creatorcontrib><creatorcontrib>Hotamisligil, Gokhan S.</creatorcontrib><title>Tumor Necrosis Factor α Mediates Apoptosis of Brown Adipocytes and Defective Brown Adipocyte Function in Obesity</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Severe quantitative and qualitative brown adipocyte defects are common in obesity. To investigate whether aberrant expression of tumor necrosis factor α (TNF-α ) in obesity is involved in functional brown fat atrophy, we have studied genetically obese (ob/ob) mice with targeted null mutations in the genes encoding the two TNF receptors. The absence of both TNF receptors or p55 receptor alone resulted in a significant reduction in brown adipocyte apoptosis and an increase in β3-adrenoreceptor and uncoupling protein-1 expression in obese mice. Increased numbers of multilocular functionally active brown adipocytes, and improved thermoregulation was also observed in obese animals lacking TNF-α function. These results indicate that TNF-α plays an important role in multiple aspects of brown adipose tissue biology and mediates the abnormalities that occur at this site in obesity.</description><subject>Adaptation, Physiological</subject><subject>Adipocytes</subject><subject>Adipocytes - cytology</subject><subject>Adipocytes - drug effects</subject><subject>Adipose Tissue, Brown - cytology</subject><subject>Adipose Tissue, Brown - drug effects</subject><subject>Animals</subject><subject>Antigens, CD - genetics</subject><subject>Apoptosis</subject><subject>b3-adrenoreceptors</subject><subject>Biological Sciences</subject><subject>Body Temperature</subject><subject>Body weight</subject><subject>Brown adipocytes</subject><subject>Brown adipose tissue</subject><subject>Carrier Proteins - metabolism</subject><subject>Cold Temperature</subject><subject>Cyclic AMP - biosynthesis</subject><subject>Genetics</subject><subject>In Situ Nick-End Labeling</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Ion Channels</subject><subject>Medical research</subject><subject>Membrane Proteins - metabolism</subject><subject>Messenger RNA</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Mitochondrial Proteins</subject><subject>Mutation</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Receptors, Adrenergic, beta - metabolism</subject><subject>Receptors, Adrenergic, beta-3</subject><subject>Receptors, Tumor Necrosis Factor - genetics</subject><subject>Receptors, Tumor Necrosis Factor, Type I</subject><subject>Receptors, Tumor Necrosis Factor, Type II</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Signal Transduction</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Uncoupling Agents - metabolism</subject><subject>Uncoupling Protein 1</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks1u1DAUhS0EokNhzQIJWSxglen1fyKxGQoDSIVuytpyEgc8ythp7BTmsXgRngmHKTDtAla2db5z7XuPEXpMYElAsZPBm7is1JLwZQmM3UELAhUpJK_gLloAUFWUnPIj9CDGDQBUooT76IhAWXLOyAJdXkzbMOKPthlDdBGvTZPy-cd3_MG2ziQb8WoIQ_olhg6_GsNXj1etG0Kzm1XjW_zadrZJ7srelvF68lkIHjuPz2sbXdo9RPc600f76Ho9Rp_Wby5O3xVn52_fn67OikZQSEXXslZSTpgkeWcr1bZMNBV0dd1JWVKiOFgOkitBK0VN3QkiKqiVJaUwomHH6OW-7jDVW9s21qfR9HoY3daMOx2M0zcV777oz-FKEymlyPbn1_YxXE42Jr11sbF9b7wNU9SKUF4q9X-QKEkkqyCDz26BmzCNPs9AUyCsFJTyDJ3soTmPONruz4MJ6DlyPUeuK6UJ13Pk2fH0sM8Dfp_xATA7f8s3Krz4J6C7qe-T_ZYy-WRPbmL-JX-vogy4YD8BwR_Keg</recordid><startdate>20000705</startdate><enddate>20000705</enddate><creator>Nisoli, Enzo</creator><creator>Briscini, Luca</creator><creator>Giordano, Antonio</creator><creator>Tonello, Cristina</creator><creator>Wiesbrock, Sarah M.</creator><creator>Uysal, K. 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Teoman</au><au>Cinti, Saverio</au><au>Carruba, Michele O.</au><au>Hotamisligil, Gokhan S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor Necrosis Factor α Mediates Apoptosis of Brown Adipocytes and Defective Brown Adipocyte Function in Obesity</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2000-07-05</date><risdate>2000</risdate><volume>97</volume><issue>14</issue><spage>8033</spage><epage>8038</epage><pages>8033-8038</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Severe quantitative and qualitative brown adipocyte defects are common in obesity. To investigate whether aberrant expression of tumor necrosis factor α (TNF-α ) in obesity is involved in functional brown fat atrophy, we have studied genetically obese (ob/ob) mice with targeted null mutations in the genes encoding the two TNF receptors. The absence of both TNF receptors or p55 receptor alone resulted in a significant reduction in brown adipocyte apoptosis and an increase in β3-adrenoreceptor and uncoupling protein-1 expression in obese mice. Increased numbers of multilocular functionally active brown adipocytes, and improved thermoregulation was also observed in obese animals lacking TNF-α function. These results indicate that TNF-α plays an important role in multiple aspects of brown adipose tissue biology and mediates the abnormalities that occur at this site in obesity.</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>10884431</pmid><doi>10.1073/pnas.97.14.8033</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Proceedings of the National Academy of Sciences - PNAS, 2000-07, Vol.97 (14), p.8033-8038 |
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| subjects | Adaptation, Physiological Adipocytes Adipocytes - cytology Adipocytes - drug effects Adipose Tissue, Brown - cytology Adipose Tissue, Brown - drug effects Animals Antigens, CD - genetics Apoptosis b3-adrenoreceptors Biological Sciences Body Temperature Body weight Brown adipocytes Brown adipose tissue Carrier Proteins - metabolism Cold Temperature Cyclic AMP - biosynthesis Genetics In Situ Nick-End Labeling Insulin Insulin resistance Ion Channels Medical research Membrane Proteins - metabolism Messenger RNA Mice Mice, Mutant Strains Mitochondrial Proteins Mutation Obesity Obesity - metabolism Receptors, Adrenergic, beta - metabolism Receptors, Adrenergic, beta-3 Receptors, Tumor Necrosis Factor - genetics Receptors, Tumor Necrosis Factor, Type I Receptors, Tumor Necrosis Factor, Type II Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Tumor Necrosis Factor-alpha - pharmacology Uncoupling Agents - metabolism Uncoupling Protein 1 |
| title | Tumor Necrosis Factor α Mediates Apoptosis of Brown Adipocytes and Defective Brown Adipocyte Function in Obesity |
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