Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: An adipokine-mediated process?
Age-dependent changes in insulin action and body fat distribution are risk factors for the development of type 2 diabetes. To examine whether the accumulation of visceral fat (VF) could play a direct role in the pathophysiology of insulin resistance and type 2 diabetes, we monitored insulin action,...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2002-10, Vol.51 (10), p.2951-2958 |
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| container_title | Diabetes (New York, N.Y.) |
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| creator | GABRIELY, Ilan XIAO HUI MA XIAO MAN YANG ATZMON, Gil RAJALA, Michael W BERG, Anders H SCHERER, Phillip ROSSETTI, Luciano BARZILAI, Nir |
| description | Age-dependent changes in insulin action and body fat distribution are risk factors for the development of type 2 diabetes. To examine whether the accumulation of visceral fat (VF) could play a direct role in the pathophysiology of insulin resistance and type 2 diabetes, we monitored insulin action, glucose tolerance, and the expression of adipo-derived peptides after surgical removal of VF in aging (20-month-old) F344/Brown Norway (FBN) and in Zucker Diabetic Fatty (ZDF) rats. As expected, peripheral and hepatic insulin action were markedly impaired in aging FBN rats, and extraction of VF (accounting for approximately 18% of their total body fat) was sufficient to restore peripheral and hepatic insulin action to the levels of young rats. When examined at the mechanistic level, removal of VF in ZDF rats prevented the progressive decrease in insulin action and delayed the onset of diabetes, but VF extraction did not alter plasma free fatty acid levels. However, the expression of tumor necrosis factor-alpha and leptin in subcutaneous (SC) adipose tissue were markedly decreased after VF removal (by approximately three- and twofold, respectively). Finally, extracted VF retained approximately 15-fold higher resistin mRNA compared with SC fat. Our data suggest that insulin resistance and the development of diabetes can be significantly reduced in aging rats by preventing the age-dependent accumulation of VF. This study documents a cause-and-effect relationship between VF and major components of the metabolic syndrome. |
| doi_str_mv | 10.2337/diabetes.51.10.2951 |
| format | Article |
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To examine whether the accumulation of visceral fat (VF) could play a direct role in the pathophysiology of insulin resistance and type 2 diabetes, we monitored insulin action, glucose tolerance, and the expression of adipo-derived peptides after surgical removal of VF in aging (20-month-old) F344/Brown Norway (FBN) and in Zucker Diabetic Fatty (ZDF) rats. As expected, peripheral and hepatic insulin action were markedly impaired in aging FBN rats, and extraction of VF (accounting for approximately 18% of their total body fat) was sufficient to restore peripheral and hepatic insulin action to the levels of young rats. When examined at the mechanistic level, removal of VF in ZDF rats prevented the progressive decrease in insulin action and delayed the onset of diabetes, but VF extraction did not alter plasma free fatty acid levels. However, the expression of tumor necrosis factor-alpha and leptin in subcutaneous (SC) adipose tissue were markedly decreased after VF removal (by approximately three- and twofold, respectively). Finally, extracted VF retained approximately 15-fold higher resistin mRNA compared with SC fat. Our data suggest that insulin resistance and the development of diabetes can be significantly reduced in aging rats by preventing the age-dependent accumulation of VF. This study documents a cause-and-effect relationship between VF and major components of the metabolic syndrome.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/diabetes.51.10.2951</identifier><identifier>PMID: 12351432</identifier><identifier>CODEN: DIAEAZ</identifier><language>eng</language><publisher>Alexandria, VA: American Diabetes Association</publisher><subject>Abdomen ; Adipose tissue ; Adipose Tissue - metabolism ; Adipose Tissue - surgery ; Adipose tissues ; Aging ; Aging (Biology) ; Aging - metabolism ; Animals ; Biological and medical sciences ; Body Composition ; Body fat ; Cardiovascular disease ; Diabetes ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - prevention & control ; Diabetes research ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Fatty Acids, Nonesterified - blood ; Gene Expression - physiology ; Glucose - metabolism ; Glucose intolerance ; Health aspects ; Hormones, Ectopic - genetics ; Insulin resistance ; Insulin Resistance - physiology ; Japanese Americans ; Leptin - genetics ; Leptin - metabolism ; Medical sciences ; Metabolism ; Nerve Growth Factor ; Obesity ; Obesity - metabolism ; Obesity - surgery ; Peptides ; Physiological aspects ; Proteins ; Rats ; Rats, Inbred BN ; Rats, Inbred F344 ; Rats, Zucker ; Resistin ; Statistics ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF</subject><ispartof>Diabetes (New York, N.Y.), 2002-10, Vol.51 (10), p.2951-2958</ispartof><rights>2003 INIST-CNRS</rights><rights>COPYRIGHT 2002 American Diabetes Association</rights><rights>Copyright American Diabetes Association Oct 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13956864$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12351432$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GABRIELY, Ilan</creatorcontrib><creatorcontrib>XIAO HUI MA</creatorcontrib><creatorcontrib>XIAO MAN YANG</creatorcontrib><creatorcontrib>ATZMON, Gil</creatorcontrib><creatorcontrib>RAJALA, Michael W</creatorcontrib><creatorcontrib>BERG, Anders H</creatorcontrib><creatorcontrib>SCHERER, Phillip</creatorcontrib><creatorcontrib>ROSSETTI, Luciano</creatorcontrib><creatorcontrib>BARZILAI, Nir</creatorcontrib><title>Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: An adipokine-mediated process?</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>Age-dependent changes in insulin action and body fat distribution are risk factors for the development of type 2 diabetes. To examine whether the accumulation of visceral fat (VF) could play a direct role in the pathophysiology of insulin resistance and type 2 diabetes, we monitored insulin action, glucose tolerance, and the expression of adipo-derived peptides after surgical removal of VF in aging (20-month-old) F344/Brown Norway (FBN) and in Zucker Diabetic Fatty (ZDF) rats. As expected, peripheral and hepatic insulin action were markedly impaired in aging FBN rats, and extraction of VF (accounting for approximately 18% of their total body fat) was sufficient to restore peripheral and hepatic insulin action to the levels of young rats. When examined at the mechanistic level, removal of VF in ZDF rats prevented the progressive decrease in insulin action and delayed the onset of diabetes, but VF extraction did not alter plasma free fatty acid levels. However, the expression of tumor necrosis factor-alpha and leptin in subcutaneous (SC) adipose tissue were markedly decreased after VF removal (by approximately three- and twofold, respectively). Finally, extracted VF retained approximately 15-fold higher resistin mRNA compared with SC fat. Our data suggest that insulin resistance and the development of diabetes can be significantly reduced in aging rats by preventing the age-dependent accumulation of VF. This study documents a cause-and-effect relationship between VF and major components of the metabolic syndrome.</description><subject>Abdomen</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - surgery</subject><subject>Adipose tissues</subject><subject>Aging</subject><subject>Aging (Biology)</subject><subject>Aging - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Body Composition</subject><subject>Body fat</subject><subject>Cardiovascular disease</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - prevention & control</subject><subject>Diabetes research</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Fatty Acids, Nonesterified - blood</subject><subject>Gene Expression - physiology</subject><subject>Glucose - metabolism</subject><subject>Glucose intolerance</subject><subject>Health aspects</subject><subject>Hormones, Ectopic - genetics</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Japanese Americans</subject><subject>Leptin - genetics</subject><subject>Leptin - metabolism</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Nerve Growth Factor</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Obesity - surgery</subject><subject>Peptides</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Inbred BN</subject><subject>Rats, Inbred F344</subject><subject>Rats, Zucker</subject><subject>Resistin</subject><subject>Statistics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kl1rFDEUhoModq3-AkEGweKFs-Zjk5l4I8tiW2GhIAreDZnkzJCaSbaTzGL_vRlcaStLORcJJ0_ec_KeIPSa4CVlrPporGohQVxyspxzkpMnaEEkkyWj1c-naIExoSWpZHWCXsR4jTEWOZ6jE0IZJytGFyh9gyHslStCV-xt1DDmfadSsRthDz7Fwvo4OeuLEaKNSXkNhfKm6N2kQ4R8nILLt-Z81lC99f2nYu0LZewu_LIeygFyqwlM1gwaYvz8Ej3rlIvw6rCeoh_nX75vLsvt1cXXzXpb9ismUklrqHinpWEV1VwI0UksW2IAGy1qTFlN21Zig40kFRWsrg2hYsU6AaplBNgpOvurmwvfTBBTM8xPdE55CFNsKkoo55Jl8O1_4HWYRp97aygRq4oQfg_qlYPG-i6kUelZsVlLyinGTGTowxGoBz8bGzx0Nqfv4-URPIeBwepj_PsHfEYS_E69mmJs6ovtI50cUB2cgx6abPTm6gH-5mDB1OaBNbvRDmq8bf59lQy8OwAqauW6eeQ23nFMclFn9_8Aig3L1A</recordid><startdate>20021001</startdate><enddate>20021001</enddate><creator>GABRIELY, Ilan</creator><creator>XIAO HUI MA</creator><creator>XIAO MAN YANG</creator><creator>ATZMON, Gil</creator><creator>RAJALA, Michael W</creator><creator>BERG, Anders H</creator><creator>SCHERER, Phillip</creator><creator>ROSSETTI, Luciano</creator><creator>BARZILAI, Nir</creator><general>American Diabetes Association</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>8GL</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20021001</creationdate><title>Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: An adipokine-mediated process?</title><author>GABRIELY, Ilan ; XIAO HUI MA ; XIAO MAN YANG ; ATZMON, Gil ; RAJALA, Michael W ; BERG, Anders H ; SCHERER, Phillip ; ROSSETTI, Luciano ; BARZILAI, Nir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g436t-28e75fc9d372c5666f909b1de0dc6802382bb90d0d91726388d12643f6eab31e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Abdomen</topic><topic>Adipose tissue</topic><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - surgery</topic><topic>Adipose tissues</topic><topic>Aging</topic><topic>Aging (Biology)</topic><topic>Aging - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Body Composition</topic><topic>Body fat</topic><topic>Cardiovascular disease</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - prevention & control</topic><topic>Diabetes research</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Fatty Acids, Nonesterified - blood</topic><topic>Gene Expression - physiology</topic><topic>Glucose - metabolism</topic><topic>Glucose intolerance</topic><topic>Health aspects</topic><topic>Hormones, Ectopic - genetics</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Japanese Americans</topic><topic>Leptin - genetics</topic><topic>Leptin - metabolism</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Nerve Growth Factor</topic><topic>Obesity</topic><topic>Obesity - metabolism</topic><topic>Obesity - surgery</topic><topic>Peptides</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Inbred BN</topic><topic>Rats, Inbred F344</topic><topic>Rats, Zucker</topic><topic>Resistin</topic><topic>Statistics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GABRIELY, Ilan</creatorcontrib><creatorcontrib>XIAO HUI MA</creatorcontrib><creatorcontrib>XIAO MAN YANG</creatorcontrib><creatorcontrib>ATZMON, Gil</creatorcontrib><creatorcontrib>RAJALA, Michael W</creatorcontrib><creatorcontrib>BERG, Anders H</creatorcontrib><creatorcontrib>SCHERER, Phillip</creatorcontrib><creatorcontrib>ROSSETTI, Luciano</creatorcontrib><creatorcontrib>BARZILAI, Nir</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Gale In Context: High School</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GABRIELY, Ilan</au><au>XIAO HUI MA</au><au>XIAO MAN YANG</au><au>ATZMON, Gil</au><au>RAJALA, Michael W</au><au>BERG, Anders H</au><au>SCHERER, Phillip</au><au>ROSSETTI, Luciano</au><au>BARZILAI, Nir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: An adipokine-mediated process?</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><addtitle>Diabetes</addtitle><date>2002-10-01</date><risdate>2002</risdate><volume>51</volume><issue>10</issue><spage>2951</spage><epage>2958</epage><pages>2951-2958</pages><issn>0012-1797</issn><eissn>1939-327X</eissn><coden>DIAEAZ</coden><abstract>Age-dependent changes in insulin action and body fat distribution are risk factors for the development of type 2 diabetes. To examine whether the accumulation of visceral fat (VF) could play a direct role in the pathophysiology of insulin resistance and type 2 diabetes, we monitored insulin action, glucose tolerance, and the expression of adipo-derived peptides after surgical removal of VF in aging (20-month-old) F344/Brown Norway (FBN) and in Zucker Diabetic Fatty (ZDF) rats. As expected, peripheral and hepatic insulin action were markedly impaired in aging FBN rats, and extraction of VF (accounting for approximately 18% of their total body fat) was sufficient to restore peripheral and hepatic insulin action to the levels of young rats. When examined at the mechanistic level, removal of VF in ZDF rats prevented the progressive decrease in insulin action and delayed the onset of diabetes, but VF extraction did not alter plasma free fatty acid levels. However, the expression of tumor necrosis factor-alpha and leptin in subcutaneous (SC) adipose tissue were markedly decreased after VF removal (by approximately three- and twofold, respectively). Finally, extracted VF retained approximately 15-fold higher resistin mRNA compared with SC fat. Our data suggest that insulin resistance and the development of diabetes can be significantly reduced in aging rats by preventing the age-dependent accumulation of VF. This study documents a cause-and-effect relationship between VF and major components of the metabolic syndrome.</abstract><cop>Alexandria, VA</cop><pub>American Diabetes Association</pub><pmid>12351432</pmid><doi>10.2337/diabetes.51.10.2951</doi><tpages>8</tpages></addata></record> |
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| ispartof | Diabetes (New York, N.Y.), 2002-10, Vol.51 (10), p.2951-2958 |
| issn | 0012-1797 1939-327X |
| language | eng |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Abdomen Adipose tissue Adipose Tissue - metabolism Adipose Tissue - surgery Adipose tissues Aging Aging (Biology) Aging - metabolism Animals Biological and medical sciences Body Composition Body fat Cardiovascular disease Diabetes Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - prevention & control Diabetes research Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Fatty Acids, Nonesterified - blood Gene Expression - physiology Glucose - metabolism Glucose intolerance Health aspects Hormones, Ectopic - genetics Insulin resistance Insulin Resistance - physiology Japanese Americans Leptin - genetics Leptin - metabolism Medical sciences Metabolism Nerve Growth Factor Obesity Obesity - metabolism Obesity - surgery Peptides Physiological aspects Proteins Rats Rats, Inbred BN Rats, Inbred F344 Rats, Zucker Resistin Statistics Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF |
| title | Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: An adipokine-mediated process? |
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