Adipose-specific peroxisome proliferator-activated receptor gamma knockout causes insulin resistance in fat and liver but not in muscle
Syndrome X, typified by obesity, insulin resistance (IR), dyslipidemia, and other metabolic abnormalities, is responsive to antidiabetic thiazolidinediones (TZDs). Peroxisome proliferator-activated receptor (PPAR) γ, a target of TZDs, is expressed abundantly in adipocytes, suggesting an important ro...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2003-12, Vol.100 (26), p.15712-15717 |
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| creator | He, W Barak, Y Hevener, A Olson, P Liao, D Le, J Nelson, M Ong, E Olefsky, J.M Evans, R.M |
| description | Syndrome X, typified by obesity, insulin resistance (IR), dyslipidemia, and other metabolic abnormalities, is responsive to antidiabetic thiazolidinediones (TZDs). Peroxisome proliferator-activated receptor (PPAR) γ, a target of TZDs, is expressed abundantly in adipocytes, suggesting an important role for this tissue in the etiology and treatment of IR. Targeted deletion of PPARγ in adipose tissue resulted in marked adipocyte hypocellularity and hypertrophy, elevated levels of plasma free fatty acids and triglyceride, and decreased levels of plasma leptin and ACRP30. In addition, increased hepatic glucogenesis and IR were observed. Despite these defects, blood glucose, glucose and insulin tolerance, and insulin-stimulated muscle glucose uptake were all comparable to those of control mice. However, targeted mice were significantly more susceptible to high-fat diet-induced steatosis, hyperinsulinemia, and IR. Surprisingly, TZD treatment effectively reversed liver IR, whereas it failed to lower plasma free fatty acids. These results suggest that syndrome X may be comprised of separable PPARγ-dependent components whose origins and therapeutic sites may reside in distinct tissues. |
| doi_str_mv | 10.1073/pnas.2536828100 |
| format | Article |
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Peroxisome proliferator-activated receptor (PPAR) γ, a target of TZDs, is expressed abundantly in adipocytes, suggesting an important role for this tissue in the etiology and treatment of IR. Targeted deletion of PPARγ in adipose tissue resulted in marked adipocyte hypocellularity and hypertrophy, elevated levels of plasma free fatty acids and triglyceride, and decreased levels of plasma leptin and ACRP30. In addition, increased hepatic glucogenesis and IR were observed. Despite these defects, blood glucose, glucose and insulin tolerance, and insulin-stimulated muscle glucose uptake were all comparable to those of control mice. However, targeted mice were significantly more susceptible to high-fat diet-induced steatosis, hyperinsulinemia, and IR. Surprisingly, TZD treatment effectively reversed liver IR, whereas it failed to lower plasma free fatty acids. These results suggest that syndrome X may be comprised of separable PPARγ-dependent components whose origins and therapeutic sites may reside in distinct tissues.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.2536828100</identifier><identifier>PMID: 14660788</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Adipocytes ; Adipocytes - physiology ; Adiponectin ; adipose tissue ; Adipose Tissue - drug effects ; Adipose Tissue - physiology ; Adipose tissues ; Animals ; Biological Sciences ; Blood ; blood glucose ; blood lipids ; Body fat ; carbohydrate metabolism ; fatty liver ; Genetics ; hypoglycemic agents ; Hypoglycemic Agents - pharmacology ; Insulin ; Insulin resistance ; Insulin Resistance - genetics ; Intercellular Signaling Peptides and Proteins ; leptin ; Leptin - blood ; Lipodystrophy - genetics ; Liver ; Liver - drug effects ; Liver - physiology ; Liver Function Tests ; metabolic syndrome ; Metabolic Syndrome - genetics ; Mice ; Mice, Knockout ; Muscle, Skeletal - drug effects ; Muscle, Skeletal - physiology ; Muscles ; mutants ; Nonesterified fatty acids ; Organ Specificity ; phenotype ; Proteins - metabolism ; Receptors, Cytoplasmic and Nuclear - deficiency ; Receptors, Cytoplasmic and Nuclear - genetics ; Rodents ; skeletal muscle ; Syndrome X ; thiazolidinedione ; thiazolidinediones ; Thiazolidinediones - pharmacology ; transcription factors ; Transcription Factors - deficiency ; Transcription Factors - genetics</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2003-12, Vol.100 (26), p.15712-15717</ispartof><rights>Copyright 1993-2003 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Dec 23, 2003</rights><rights>Copyright © 2003, The National Academy of Sciences 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c550t-93b5f33e2040efa5f5fe722877caa1422dc43b44172491bd786a268588c405c33</citedby><cites>FETCH-LOGICAL-c550t-93b5f33e2040efa5f5fe722877caa1422dc43b44172491bd786a268588c405c33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/100/26.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3149071$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3149071$$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/14660788$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, W</creatorcontrib><creatorcontrib>Barak, Y</creatorcontrib><creatorcontrib>Hevener, A</creatorcontrib><creatorcontrib>Olson, P</creatorcontrib><creatorcontrib>Liao, D</creatorcontrib><creatorcontrib>Le, J</creatorcontrib><creatorcontrib>Nelson, M</creatorcontrib><creatorcontrib>Ong, E</creatorcontrib><creatorcontrib>Olefsky, J.M</creatorcontrib><creatorcontrib>Evans, R.M</creatorcontrib><title>Adipose-specific peroxisome proliferator-activated receptor gamma knockout causes insulin resistance in fat and liver but not in muscle</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Syndrome X, typified by obesity, insulin resistance (IR), dyslipidemia, and other metabolic abnormalities, is responsive to antidiabetic thiazolidinediones (TZDs). Peroxisome proliferator-activated receptor (PPAR) γ, a target of TZDs, is expressed abundantly in adipocytes, suggesting an important role for this tissue in the etiology and treatment of IR. Targeted deletion of PPARγ in adipose tissue resulted in marked adipocyte hypocellularity and hypertrophy, elevated levels of plasma free fatty acids and triglyceride, and decreased levels of plasma leptin and ACRP30. In addition, increased hepatic glucogenesis and IR were observed. Despite these defects, blood glucose, glucose and insulin tolerance, and insulin-stimulated muscle glucose uptake were all comparable to those of control mice. However, targeted mice were significantly more susceptible to high-fat diet-induced steatosis, hyperinsulinemia, and IR. Surprisingly, TZD treatment effectively reversed liver IR, whereas it failed to lower plasma free fatty acids. These results suggest that syndrome X may be comprised of separable PPARγ-dependent components whose origins and therapeutic sites may reside in distinct tissues.</description><subject>Adipocytes</subject><subject>Adipocytes - physiology</subject><subject>Adiponectin</subject><subject>adipose tissue</subject><subject>Adipose Tissue - drug effects</subject><subject>Adipose Tissue - physiology</subject><subject>Adipose tissues</subject><subject>Animals</subject><subject>Biological Sciences</subject><subject>Blood</subject><subject>blood glucose</subject><subject>blood lipids</subject><subject>Body fat</subject><subject>carbohydrate metabolism</subject><subject>fatty liver</subject><subject>Genetics</subject><subject>hypoglycemic agents</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>leptin</subject><subject>Leptin - blood</subject><subject>Lipodystrophy - genetics</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - physiology</subject><subject>Liver Function Tests</subject><subject>metabolic syndrome</subject><subject>Metabolic Syndrome - genetics</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Muscle, Skeletal - drug effects</subject><subject>Muscle, Skeletal - physiology</subject><subject>Muscles</subject><subject>mutants</subject><subject>Nonesterified fatty acids</subject><subject>Organ Specificity</subject><subject>phenotype</subject><subject>Proteins - metabolism</subject><subject>Receptors, Cytoplasmic and Nuclear - deficiency</subject><subject>Receptors, Cytoplasmic and Nuclear - genetics</subject><subject>Rodents</subject><subject>skeletal muscle</subject><subject>Syndrome X</subject><subject>thiazolidinedione</subject><subject>thiazolidinediones</subject><subject>Thiazolidinediones - pharmacology</subject><subject>transcription factors</subject><subject>Transcription Factors - deficiency</subject><subject>Transcription Factors - genetics</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkktv1DAUhSMEokNhzQaBxQKJRdrrV-wsuqgqXlIlFtC15XHswdMkDrYzKr-Av42jGXWATVeW7vnOta_vqaqXGM4wCHo-jTqdEU4bSSQGeFStMLS4blgLj6sVABG1ZISdVM9S2gJAyyU8rU4waxoQUq6q35edn0KydZqs8c4bNNkY7nwKg0VTDL13NuocYq1N9judbYeiNXYqJbTRw6DR7RjMbZgzMnpONiE_prn3Y8GST1mPxpYScjojPXao9zsb0brgY8iLMMzJ9PZ59cTpPtkXh_O0uvn44fvV5_r666cvV5fXteEcct3SNXeUWgIMrNPccWcFIVIIozVmhHSG0TVjWBDW4nUnZKNJI7mUhgE3lJ5WF_u-07webGfsmKPu1RT9oOMvFbRX_yqj_6E2YacoiIYu_ncHfww_Z5uyGnwytu_1aMOclMBMCiLgQRC3pOyiWcC3_4HbMMexfIIigBljnC_Xnu8hE0NK0br7F2NQSxLUkgR1TEJxvP570CN_WH0B0AFYnMd2oEijMBeYFOT9A4hyc99ne5cL-2rPblOJxj1McYmiwEV-s5edDkpvok_q5luZjwKGBlMO9A9m590x</recordid><startdate>20031223</startdate><enddate>20031223</enddate><creator>He, W</creator><creator>Barak, Y</creator><creator>Hevener, A</creator><creator>Olson, P</creator><creator>Liao, D</creator><creator>Le, J</creator><creator>Nelson, M</creator><creator>Ong, E</creator><creator>Olefsky, J.M</creator><creator>Evans, R.M</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</scope><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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20031223</creationdate><title>Adipose-specific peroxisome proliferator-activated receptor gamma knockout causes insulin resistance in fat and liver but not in muscle</title><author>He, W ; Barak, Y ; Hevener, A ; Olson, P ; Liao, D ; Le, J ; Nelson, M ; Ong, E ; Olefsky, J.M ; Evans, R.M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c550t-93b5f33e2040efa5f5fe722877caa1422dc43b44172491bd786a268588c405c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adipocytes</topic><topic>Adipocytes - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, W</au><au>Barak, Y</au><au>Hevener, A</au><au>Olson, P</au><au>Liao, D</au><au>Le, J</au><au>Nelson, M</au><au>Ong, E</au><au>Olefsky, J.M</au><au>Evans, R.M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adipose-specific peroxisome proliferator-activated receptor gamma knockout causes insulin resistance in fat and liver but not in muscle</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2003-12-23</date><risdate>2003</risdate><volume>100</volume><issue>26</issue><spage>15712</spage><epage>15717</epage><pages>15712-15717</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Syndrome X, typified by obesity, insulin resistance (IR), dyslipidemia, and other metabolic abnormalities, is responsive to antidiabetic thiazolidinediones (TZDs). Peroxisome proliferator-activated receptor (PPAR) γ, a target of TZDs, is expressed abundantly in adipocytes, suggesting an important role for this tissue in the etiology and treatment of IR. Targeted deletion of PPARγ in adipose tissue resulted in marked adipocyte hypocellularity and hypertrophy, elevated levels of plasma free fatty acids and triglyceride, and decreased levels of plasma leptin and ACRP30. In addition, increased hepatic glucogenesis and IR were observed. Despite these defects, blood glucose, glucose and insulin tolerance, and insulin-stimulated muscle glucose uptake were all comparable to those of control mice. However, targeted mice were significantly more susceptible to high-fat diet-induced steatosis, hyperinsulinemia, and IR. Surprisingly, TZD treatment effectively reversed liver IR, whereas it failed to lower plasma free fatty acids. These results suggest that syndrome X may be comprised of separable PPARγ-dependent components whose origins and therapeutic sites may reside in distinct tissues.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>14660788</pmid><doi>10.1073/pnas.2536828100</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes Adipocytes - physiology Adiponectin adipose tissue Adipose Tissue - drug effects Adipose Tissue - physiology Adipose tissues Animals Biological Sciences Blood blood glucose blood lipids Body fat carbohydrate metabolism fatty liver Genetics hypoglycemic agents Hypoglycemic Agents - pharmacology Insulin Insulin resistance Insulin Resistance - genetics Intercellular Signaling Peptides and Proteins leptin Leptin - blood Lipodystrophy - genetics Liver Liver - drug effects Liver - physiology Liver Function Tests metabolic syndrome Metabolic Syndrome - genetics Mice Mice, Knockout Muscle, Skeletal - drug effects Muscle, Skeletal - physiology Muscles mutants Nonesterified fatty acids Organ Specificity phenotype Proteins - metabolism Receptors, Cytoplasmic and Nuclear - deficiency Receptors, Cytoplasmic and Nuclear - genetics Rodents skeletal muscle Syndrome X thiazolidinedione thiazolidinediones Thiazolidinediones - pharmacology transcription factors Transcription Factors - deficiency Transcription Factors - genetics |
| title | Adipose-specific peroxisome proliferator-activated receptor gamma knockout causes insulin resistance in fat and liver but not in muscle |
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