Preadipocytes of type 2 diabetes subjects display an intrinsic gene expression profile of decreased differentiation capacity
Objective: Insulin resistance and type 2 diabetes mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. In this study, we identified the underlying molecular processes in preadipocytes of T2DM patients, a characteristi...
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| Veröffentlicht in: | International Journal of Obesity 2011-09, Vol.35 (9), p.1154-1164 |
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| creator | Tienen, F.H.J van Kallen, C.J.H. van der Lindsey, P.J Wanders, R.J Greevenbroek, M.M. van Smeets, H.J.M |
| description | Objective: Insulin resistance and type 2 diabetes mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. In this study, we identified the underlying molecular processes in preadipocytes of T2DM patients, a characteristic for the development of T2DM. Design and Participants: Preadipocyte cell cultures were prepared from subcutaneous fat biopsies of seven T2DM patients (age 53+/-12 years; body mass index (BMI) 34+/-5 kg m-2) and nine control subjects (age 51+/-12 years; BMI 30+/-3 kg m-2). Microarray analysis was used to identify altered processes between the T2DM and control preadipocytes. Results: Gene expression profiling showed changed expression of transcription regulators involved in adipogenesis and in extracellular matrix remodeling, actin cytoskeleton and integrin signaling genes, which indicated decreased capacity to differentiate. Additionally, genes involved in insulin signaling and lipid metabolism were downregulated, and inflammation/apoptosis was upregulated in T2DM preadipocytes. Conclusion: Decreased expression of genes involved in differentiation can provide a molecular basis for the reduced adipogenesis of preadipocytes of T2DM subjects, leading to reduced formation of adipocytes in subcutaneous fat depots, and ultimately leading to ectopic fat storage. |
| doi_str_mv | 10.1038/ijo.2010.275 |
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In this study, we identified the underlying molecular processes in preadipocytes of T2DM patients, a characteristic for the development of T2DM. Design and Participants: Preadipocyte cell cultures were prepared from subcutaneous fat biopsies of seven T2DM patients (age 53+/-12 years; body mass index (BMI) 34+/-5 kg m-2) and nine control subjects (age 51+/-12 years; BMI 30+/-3 kg m-2). Microarray analysis was used to identify altered processes between the T2DM and control preadipocytes. Results: Gene expression profiling showed changed expression of transcription regulators involved in adipogenesis and in extracellular matrix remodeling, actin cytoskeleton and integrin signaling genes, which indicated decreased capacity to differentiate. Additionally, genes involved in insulin signaling and lipid metabolism were downregulated, and inflammation/apoptosis was upregulated in T2DM preadipocytes. Conclusion: Decreased expression of genes involved in differentiation can provide a molecular basis for the reduced adipogenesis of preadipocytes of T2DM subjects, leading to reduced formation of adipocytes in subcutaneous fat depots, and ultimately leading to ectopic fat storage.</description><identifier>ISSN: 0307-0565</identifier><identifier>EISSN: 1476-5497</identifier><identifier>DOI: 10.1038/ijo.2010.275</identifier><identifier>PMID: 21326205</identifier><identifier>CODEN: IJOBDP</identifier><language>eng</language><publisher>London: Nature Publishing Group</publisher><subject>631/136/142 ; 631/208/191/2018 ; 692/699/2743/137/773 ; 692/699/2743/393 ; Actin ; Adipocytes ; Adipocytes - pathology ; adipogenesis ; Adipogenesis - genetics ; Adipose Tissue - pathology ; Age ; Apoptosis ; Biological and medical sciences ; Biology ; Biopsy ; Body fat ; Body Mass Index ; Cell culture ; Cell Differentiation ; Cells, Cultured ; Cytoskeleton ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - pathology ; Diabetes. Impaired glucose tolerance ; Diagnosis ; Differentiation ; DNA microarrays ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Epidemiology ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Extracellular matrix ; Female ; Gene expression ; Gene Expression Profiling ; gene expression regulation ; genes ; Genetic aspects ; Health Promotion and Disease Prevention ; Humans ; Inflammation ; Insulin ; Insulin resistance ; Integrins ; Internal Medicine ; Lipid metabolism ; Lipids ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolic disorders ; Microarray Analysis ; microarray technology ; microfilaments ; Middle Aged ; noninsulin-dependent diabetes mellitus ; Obesity ; original-article ; patients ; Physiological aspects ; Preadipocytes ; Proteins ; Public Health ; subcutaneous fat ; Transcription ; Transcription, Genetic ; Type 2 diabetes</subject><ispartof>International Journal of Obesity, 2011-09, Vol.35 (9), p.1154-1164</ispartof><rights>Macmillan Publishers Limited 2011</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2011 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-585e779a4314d30bb6f2138f09910d1902b9e54d31c0c72f9773dfcdc519376c3</citedby><cites>FETCH-LOGICAL-c540t-585e779a4314d30bb6f2138f09910d1902b9e54d31c0c72f9773dfcdc519376c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ijo.2010.275$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ijo.2010.275$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24487923$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21326205$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tienen, F.H.J van</creatorcontrib><creatorcontrib>Kallen, C.J.H. van der</creatorcontrib><creatorcontrib>Lindsey, P.J</creatorcontrib><creatorcontrib>Wanders, R.J</creatorcontrib><creatorcontrib>Greevenbroek, M.M. van</creatorcontrib><creatorcontrib>Smeets, H.J.M</creatorcontrib><title>Preadipocytes of type 2 diabetes subjects display an intrinsic gene expression profile of decreased differentiation capacity</title><title>International Journal of Obesity</title><addtitle>Int J Obes</addtitle><addtitle>Int J Obes (Lond)</addtitle><description>Objective: Insulin resistance and type 2 diabetes mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. In this study, we identified the underlying molecular processes in preadipocytes of T2DM patients, a characteristic for the development of T2DM. Design and Participants: Preadipocyte cell cultures were prepared from subcutaneous fat biopsies of seven T2DM patients (age 53+/-12 years; body mass index (BMI) 34+/-5 kg m-2) and nine control subjects (age 51+/-12 years; BMI 30+/-3 kg m-2). Microarray analysis was used to identify altered processes between the T2DM and control preadipocytes. Results: Gene expression profiling showed changed expression of transcription regulators involved in adipogenesis and in extracellular matrix remodeling, actin cytoskeleton and integrin signaling genes, which indicated decreased capacity to differentiate. Additionally, genes involved in insulin signaling and lipid metabolism were downregulated, and inflammation/apoptosis was upregulated in T2DM preadipocytes. Conclusion: Decreased expression of genes involved in differentiation can provide a molecular basis for the reduced adipogenesis of preadipocytes of T2DM subjects, leading to reduced formation of adipocytes in subcutaneous fat depots, and ultimately leading to ectopic fat storage.</description><subject>631/136/142</subject><subject>631/208/191/2018</subject><subject>692/699/2743/137/773</subject><subject>692/699/2743/393</subject><subject>Actin</subject><subject>Adipocytes</subject><subject>Adipocytes - pathology</subject><subject>adipogenesis</subject><subject>Adipogenesis - genetics</subject><subject>Adipose Tissue - pathology</subject><subject>Age</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Biology</subject><subject>Biopsy</subject><subject>Body fat</subject><subject>Body Mass Index</subject><subject>Cell culture</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Cytoskeleton</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diagnosis</subject><subject>Differentiation</subject><subject>DNA microarrays</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Epidemiology</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Extracellular matrix</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>gene expression regulation</subject><subject>genes</subject><subject>Genetic aspects</subject><subject>Health Promotion and Disease Prevention</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Integrins</subject><subject>Internal Medicine</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolic disorders</subject><subject>Microarray Analysis</subject><subject>microarray technology</subject><subject>microfilaments</subject><subject>Middle Aged</subject><subject>noninsulin-dependent diabetes mellitus</subject><subject>Obesity</subject><subject>original-article</subject><subject>patients</subject><subject>Physiological aspects</subject><subject>Preadipocytes</subject><subject>Proteins</subject><subject>Public Health</subject><subject>subcutaneous fat</subject><subject>Transcription</subject><subject>Transcription, Genetic</subject><subject>Type 2 diabetes</subject><issn>0307-0565</issn><issn>1476-5497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9ktuL1DAUxoMo7jr65rMWxcuDHdNcmuZxWbzBgoLuc0nTk9kMnaQmLTjgH-8pM7quqOQhJOd3vuR8fIQ8rOi6orx57bdxzSiemJK3yGklVF1KodVtcko5VSWVtTwh93LeUkqlpOwuOWEVZzWj8pR8_5TA9H6Mdj9BLqIrpv0IBSt6bzpYrvLcbcFOGW_yOJh9YULhw5R8yN4WGwhQwLcxQc4-hmJM0fkBFqEeLGpn6LHTOUgQJm-mBbJmNNZP-_vkjjNDhgfHfUUu3775cv6-vPj47sP52UVppaBTKRsJSmkjeCV6TruudjhA46jWFe0rTVmnQWKpstQq5rRSvHe2t7LSXNWWr8iLgy7-7usMeWp3PlsYBhMgzrltGi1kRVF0RV7-l0SIyZqj8Yg--QPdxjkFnAP1GsVlpShCTw_QxgzQ-uDilIxdNNszVjdC6VoIpNZ_oXD1sPM2Blgsvdnw_LeGKzDDdJXjMC_u5pvgqwNoU8w5gWvH5Hcm7XGSdolPi_Fpl_i0GB_EHx1nmrsd9L_gn3lB4NkRMNmawSUTrM_XnBCN0mwxpzxwGUthA-nanH88_PjAOxNbs0moefkZqxIzq7jQmv8Ai87jHg</recordid><startdate>20110901</startdate><enddate>20110901</enddate><creator>Tienen, F.H.J van</creator><creator>Kallen, C.J.H. van der</creator><creator>Lindsey, P.J</creator><creator>Wanders, R.J</creator><creator>Greevenbroek, M.M. van</creator><creator>Smeets, H.J.M</creator><general>Nature Publishing Group</general><general>Nature Publishing Group UK</general><scope>FBQ</scope><scope>IQODW</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>3V.</scope><scope>7T2</scope><scope>7TK</scope><scope>7TS</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20110901</creationdate><title>Preadipocytes of type 2 diabetes subjects display an intrinsic gene expression profile of decreased differentiation capacity</title><author>Tienen, F.H.J van ; Kallen, C.J.H. van der ; Lindsey, P.J ; Wanders, R.J ; Greevenbroek, M.M. van ; Smeets, H.J.M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-585e779a4314d30bb6f2138f09910d1902b9e54d31c0c72f9773dfcdc519376c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>631/136/142</topic><topic>631/208/191/2018</topic><topic>692/699/2743/137/773</topic><topic>692/699/2743/393</topic><topic>Actin</topic><topic>Adipocytes</topic><topic>Adipocytes - pathology</topic><topic>adipogenesis</topic><topic>Adipogenesis - genetics</topic><topic>Adipose Tissue - pathology</topic><topic>Age</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Biology</topic><topic>Biopsy</topic><topic>Body fat</topic><topic>Body Mass Index</topic><topic>Cell culture</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>Cytoskeleton</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diagnosis</topic><topic>Differentiation</topic><topic>DNA microarrays</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Epidemiology</topic><topic>Etiopathogenesis. Screening. Investigations. 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Academic</collection><jtitle>International Journal of Obesity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tienen, F.H.J van</au><au>Kallen, C.J.H. van der</au><au>Lindsey, P.J</au><au>Wanders, R.J</au><au>Greevenbroek, M.M. van</au><au>Smeets, H.J.M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preadipocytes of type 2 diabetes subjects display an intrinsic gene expression profile of decreased differentiation capacity</atitle><jtitle>International Journal of Obesity</jtitle><stitle>Int J Obes</stitle><addtitle>Int J Obes (Lond)</addtitle><date>2011-09-01</date><risdate>2011</risdate><volume>35</volume><issue>9</issue><spage>1154</spage><epage>1164</epage><pages>1154-1164</pages><issn>0307-0565</issn><eissn>1476-5497</eissn><coden>IJOBDP</coden><abstract>Objective: Insulin resistance and type 2 diabetes mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. In this study, we identified the underlying molecular processes in preadipocytes of T2DM patients, a characteristic for the development of T2DM. Design and Participants: Preadipocyte cell cultures were prepared from subcutaneous fat biopsies of seven T2DM patients (age 53+/-12 years; body mass index (BMI) 34+/-5 kg m-2) and nine control subjects (age 51+/-12 years; BMI 30+/-3 kg m-2). Microarray analysis was used to identify altered processes between the T2DM and control preadipocytes. Results: Gene expression profiling showed changed expression of transcription regulators involved in adipogenesis and in extracellular matrix remodeling, actin cytoskeleton and integrin signaling genes, which indicated decreased capacity to differentiate. Additionally, genes involved in insulin signaling and lipid metabolism were downregulated, and inflammation/apoptosis was upregulated in T2DM preadipocytes. Conclusion: Decreased expression of genes involved in differentiation can provide a molecular basis for the reduced adipogenesis of preadipocytes of T2DM subjects, leading to reduced formation of adipocytes in subcutaneous fat depots, and ultimately leading to ectopic fat storage.</abstract><cop>London</cop><pub>Nature Publishing Group</pub><pmid>21326205</pmid><doi>10.1038/ijo.2010.275</doi><tpages>11</tpages></addata></record> |
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| subjects | 631/136/142 631/208/191/2018 692/699/2743/137/773 692/699/2743/393 Actin Adipocytes Adipocytes - pathology adipogenesis Adipogenesis - genetics Adipose Tissue - pathology Age Apoptosis Biological and medical sciences Biology Biopsy Body fat Body Mass Index Cell culture Cell Differentiation Cells, Cultured Cytoskeleton Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - pathology Diabetes. Impaired glucose tolerance Diagnosis Differentiation DNA microarrays Endocrine pancreas. Apud cells (diseases) Endocrinopathies Epidemiology Etiopathogenesis. Screening. Investigations. Target tissue resistance Extracellular matrix Female Gene expression Gene Expression Profiling gene expression regulation genes Genetic aspects Health Promotion and Disease Prevention Humans Inflammation Insulin Insulin resistance Integrins Internal Medicine Lipid metabolism Lipids Male Medical sciences Medicine Medicine & Public Health Metabolic Diseases Metabolic disorders Microarray Analysis microarray technology microfilaments Middle Aged noninsulin-dependent diabetes mellitus Obesity original-article patients Physiological aspects Preadipocytes Proteins Public Health subcutaneous fat Transcription Transcription, Genetic Type 2 diabetes |
| title | Preadipocytes of type 2 diabetes subjects display an intrinsic gene expression profile of decreased differentiation capacity |
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