Whole blood gene expression profiles in insulin resistant Latinos with the metabolic syndrome
Although insulin resistance in skeletal muscle is well-characterized, the role of circulating whole blood in the metabolic syndrome phenotype is not well understood. We set out to test the hypothesis that genes involved in inflammation, insulin signaling and mitochondrial function would be altered i...
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| creator | Tangen, Samantha E Tsinajinnie, Darwin Nuñez, Martha Shaibi, Gabriel Q Mandarino, Lawrence J Coletta, Dawn K |
| description | Although insulin resistance in skeletal muscle is well-characterized, the role of circulating whole blood in the metabolic syndrome phenotype is not well understood. We set out to test the hypothesis that genes involved in inflammation, insulin signaling and mitochondrial function would be altered in expression in the whole blood of individuals with metabolic syndrome. We further wanted to examine whether similar relationships that we have found previously in skeletal muscle exist in peripheral whole blood cells. All subjects (n=184) were Latino descent from the Arizona Insulin Resistance registry. Subjects were classified based on the metabolic syndrome phenotype according to the National Cholesterol Education Program's Adult Treatment Panel III. Of the 184 Latino subjects in the study, 74 were classified with the metabolic syndrome and 110 were without. Whole blood gene expression profiling was performed using the Agilent 4x44K Whole Human Genome Microarray. Whole blood microarray analysis identified 1,432 probes that were altered in expression ≥ 1.2 fold and P |
| doi_str_mv | 10.1371/journal.pone.0084002 |
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We set out to test the hypothesis that genes involved in inflammation, insulin signaling and mitochondrial function would be altered in expression in the whole blood of individuals with metabolic syndrome. We further wanted to examine whether similar relationships that we have found previously in skeletal muscle exist in peripheral whole blood cells. All subjects (n=184) were Latino descent from the Arizona Insulin Resistance registry. Subjects were classified based on the metabolic syndrome phenotype according to the National Cholesterol Education Program's Adult Treatment Panel III. Of the 184 Latino subjects in the study, 74 were classified with the metabolic syndrome and 110 were without. Whole blood gene expression profiling was performed using the Agilent 4x44K Whole Human Genome Microarray. Whole blood microarray analysis identified 1,432 probes that were altered in expression ≥ 1.2 fold and P<0.05 after Benjamini-Hochberg in the metabolic syndrome subjects. KEGG pathway analysis revealed significant enrichment for pathways including ribosome, oxidative phosphorylation and MAPK signaling (all Benjamini-Hochberg P<0.05). Whole blood mRNA expression changes observed in the microarray data were confirmed by quantitative RT-PCR. Transcription factor binding motif enrichment analysis revealed E2F1, ELK1, NF-kappaB, STAT1 and STAT3 significantly enriched after Bonferroni correction (all P<0.05). The results of the present study demonstrate that whole blood is a useful tissue for studying the metabolic syndrome and its underlying insulin resistance although the relationship between blood and skeletal muscle differs.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0084002</identifier><identifier>PMID: 24358323</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Analysis ; Arizona ; Binding Sites ; Blood ; Blood cells ; Blood circulation ; Cholesterol ; Diabetes ; DNA microarrays ; DNA probes ; Enrichment ; Family medical history ; Female ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genes ; Genomes ; Glucose ; Hispanic Americans ; Hispanic Americans - genetics ; Humans ; Hybridization ; Hypertension ; Hypotheses ; Inflammation ; Insulin ; Insulin resistance ; Insulin Resistance - genetics ; Kinases ; Life sciences ; Lupus ; Male ; MAP kinase ; Metabolic disorders ; Metabolic Networks and Pathways ; Metabolic syndrome ; Metabolic Syndrome - genetics ; Metabolic Syndrome - metabolism ; Metabolites ; Mitochondria ; Muscles ; Musculoskeletal system ; NF-κB protein ; Nucleotide Motifs ; Obesity ; Oxidative phosphorylation ; Phosphorylation ; Polymerase chain reaction ; Registries ; Risk Factors ; RNA ; Signal transduction ; Signaling ; Skeletal muscle ; Stat1 protein ; Stat3 protein ; Transcription Factors - metabolism ; Transcriptome ; Type 2 diabetes ; Womens health</subject><ispartof>PloS one, 2013-12, Vol.8 (12), p.e84002-e84002</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Tangen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Tangen et al 2013 Tangen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-e5410378aaf9a6af81f09f4b39002f02bea220f0f14f213eaca3c2373e9cf6b63</citedby><cites>FETCH-LOGICAL-c692t-e5410378aaf9a6af81f09f4b39002f02bea220f0f14f213eaca3c2373e9cf6b63</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/PMC3866261/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3866261/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24358323$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tangen, Samantha E</creatorcontrib><creatorcontrib>Tsinajinnie, Darwin</creatorcontrib><creatorcontrib>Nuñez, Martha</creatorcontrib><creatorcontrib>Shaibi, Gabriel Q</creatorcontrib><creatorcontrib>Mandarino, Lawrence J</creatorcontrib><creatorcontrib>Coletta, Dawn K</creatorcontrib><title>Whole blood gene expression profiles in insulin resistant Latinos with the metabolic syndrome</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Although insulin resistance in skeletal muscle is well-characterized, the role of circulating whole blood in the metabolic syndrome phenotype is not well understood. We set out to test the hypothesis that genes involved in inflammation, insulin signaling and mitochondrial function would be altered in expression in the whole blood of individuals with metabolic syndrome. We further wanted to examine whether similar relationships that we have found previously in skeletal muscle exist in peripheral whole blood cells. All subjects (n=184) were Latino descent from the Arizona Insulin Resistance registry. Subjects were classified based on the metabolic syndrome phenotype according to the National Cholesterol Education Program's Adult Treatment Panel III. Of the 184 Latino subjects in the study, 74 were classified with the metabolic syndrome and 110 were without. Whole blood gene expression profiling was performed using the Agilent 4x44K Whole Human Genome Microarray. Whole blood microarray analysis identified 1,432 probes that were altered in expression ≥ 1.2 fold and P<0.05 after Benjamini-Hochberg in the metabolic syndrome subjects. KEGG pathway analysis revealed significant enrichment for pathways including ribosome, oxidative phosphorylation and MAPK signaling (all Benjamini-Hochberg P<0.05). Whole blood mRNA expression changes observed in the microarray data were confirmed by quantitative RT-PCR. Transcription factor binding motif enrichment analysis revealed E2F1, ELK1, NF-kappaB, STAT1 and STAT3 significantly enriched after Bonferroni correction (all P<0.05). The results of the present study demonstrate that whole blood is a useful tissue for studying the metabolic syndrome and its underlying insulin resistance although the relationship between blood and skeletal muscle differs.</description><subject>Adult</subject><subject>Analysis</subject><subject>Arizona</subject><subject>Binding Sites</subject><subject>Blood</subject><subject>Blood cells</subject><subject>Blood circulation</subject><subject>Cholesterol</subject><subject>Diabetes</subject><subject>DNA microarrays</subject><subject>DNA probes</subject><subject>Enrichment</subject><subject>Family medical history</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Genomes</subject><subject>Glucose</subject><subject>Hispanic Americans</subject><subject>Hispanic Americans - genetics</subject><subject>Humans</subject><subject>Hybridization</subject><subject>Hypertension</subject><subject>Hypotheses</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Kinases</subject><subject>Life sciences</subject><subject>Lupus</subject><subject>Male</subject><subject>MAP kinase</subject><subject>Metabolic disorders</subject><subject>Metabolic Networks and Pathways</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - genetics</subject><subject>Metabolic Syndrome - metabolism</subject><subject>Metabolites</subject><subject>Mitochondria</subject><subject>Muscles</subject><subject>Musculoskeletal system</subject><subject>NF-κB protein</subject><subject>Nucleotide Motifs</subject><subject>Obesity</subject><subject>Oxidative phosphorylation</subject><subject>Phosphorylation</subject><subject>Polymerase chain reaction</subject><subject>Registries</subject><subject>Risk Factors</subject><subject>RNA</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Skeletal muscle</subject><subject>Stat1 protein</subject><subject>Stat3 protein</subject><subject>Transcription Factors - metabolism</subject><subject>Transcriptome</subject><subject>Type 2 diabetes</subject><subject>Womens 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blood gene expression profiles in insulin resistant Latinos with the metabolic syndrome</title><author>Tangen, Samantha E ; Tsinajinnie, Darwin ; Nuñez, Martha ; Shaibi, Gabriel Q ; Mandarino, Lawrence J ; Coletta, Dawn K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-e5410378aaf9a6af81f09f4b39002f02bea220f0f14f213eaca3c2373e9cf6b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Analysis</topic><topic>Arizona</topic><topic>Binding Sites</topic><topic>Blood</topic><topic>Blood cells</topic><topic>Blood circulation</topic><topic>Cholesterol</topic><topic>Diabetes</topic><topic>DNA microarrays</topic><topic>DNA probes</topic><topic>Enrichment</topic><topic>Family medical history</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression 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One</addtitle><date>2013-12-17</date><risdate>2013</risdate><volume>8</volume><issue>12</issue><spage>e84002</spage><epage>e84002</epage><pages>e84002-e84002</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Although insulin resistance in skeletal muscle is well-characterized, the role of circulating whole blood in the metabolic syndrome phenotype is not well understood. We set out to test the hypothesis that genes involved in inflammation, insulin signaling and mitochondrial function would be altered in expression in the whole blood of individuals with metabolic syndrome. We further wanted to examine whether similar relationships that we have found previously in skeletal muscle exist in peripheral whole blood cells. All subjects (n=184) were Latino descent from the Arizona Insulin Resistance registry. Subjects were classified based on the metabolic syndrome phenotype according to the National Cholesterol Education Program's Adult Treatment Panel III. Of the 184 Latino subjects in the study, 74 were classified with the metabolic syndrome and 110 were without. Whole blood gene expression profiling was performed using the Agilent 4x44K Whole Human Genome Microarray. Whole blood microarray analysis identified 1,432 probes that were altered in expression ≥ 1.2 fold and P<0.05 after Benjamini-Hochberg in the metabolic syndrome subjects. KEGG pathway analysis revealed significant enrichment for pathways including ribosome, oxidative phosphorylation and MAPK signaling (all Benjamini-Hochberg P<0.05). Whole blood mRNA expression changes observed in the microarray data were confirmed by quantitative RT-PCR. Transcription factor binding motif enrichment analysis revealed E2F1, ELK1, NF-kappaB, STAT1 and STAT3 significantly enriched after Bonferroni correction (all P<0.05). The results of the present study demonstrate that whole blood is a useful tissue for studying the metabolic syndrome and its underlying insulin resistance although the relationship between blood and skeletal muscle differs.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24358323</pmid><doi>10.1371/journal.pone.0084002</doi><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adult Analysis Arizona Binding Sites Blood Blood cells Blood circulation Cholesterol Diabetes DNA microarrays DNA probes Enrichment Family medical history Female Gene expression Gene Expression Profiling Gene Expression Regulation Genes Genomes Glucose Hispanic Americans Hispanic Americans - genetics Humans Hybridization Hypertension Hypotheses Inflammation Insulin Insulin resistance Insulin Resistance - genetics Kinases Life sciences Lupus Male MAP kinase Metabolic disorders Metabolic Networks and Pathways Metabolic syndrome Metabolic Syndrome - genetics Metabolic Syndrome - metabolism Metabolites Mitochondria Muscles Musculoskeletal system NF-κB protein Nucleotide Motifs Obesity Oxidative phosphorylation Phosphorylation Polymerase chain reaction Registries Risk Factors RNA Signal transduction Signaling Skeletal muscle Stat1 protein Stat3 protein Transcription Factors - metabolism Transcriptome Type 2 diabetes Womens health |
| title | Whole blood gene expression profiles in insulin resistant Latinos with the metabolic syndrome |
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