<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Olsson M</submitter><funding>Swedish Diabetes foundation</funding><funding>VINNOVA-VINNMER program</funding><funding>Royal Physiographic Society (Nilsson-Ehle foundation)</funding><funding>Magnus Bergvall foundation</funding><funding>Swedish Research Council</funding><funding>Swedish Knowledge Foundation through</funding><funding>the Swedish foundation for Strategic Research to Sahlgrenska Center for Cardiovascular and Metabolic Research,</funding><funding>Åke Wiberg foundation</funding><funding>Tore Nilson foundation</funding><funding>Jeansson foundations</funding><funding>Medical Research Council</funding><funding>Wellcome Trust</funding><funding>foundations of the National Board of Health and Welfare</funding><funding>Swedish federal government</funding><pagination>114-20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3004038</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>60(1)</volume><pubmed_abstract>The selenoprotein S (SELS) is a putative receptor for serum amyloid A, and recent studies have suggested that SELS may be a link between type 2 diabetes mellitus and inflammation. Genetic studies of SELS polymorphisms have revealed associations with circulating levels of inflammatory markers and hard end points of cardiovascular disease. In this study, we analyzed SELS expression in subcutaneous adipose tissue and SELS genotype in relation to metabolic risk factors. DNA microarray expression analysis was used to study the expression of SELS in lean and obese siblings from the Swedish Obese Subjects Sib Pair Study. TaqMan genotyping was used to analyze 3 polymorphisms, previously found to be associated with circulating levels of inflammatory markers, in the INTERGENE case-control study of m</pubmed_abstract><journal>Metabolism: clinical and experimental</journal><pubmed_title>Expression of the selenoprotein S (SELS) gene in subcutaneous adipose tissue and SELS genotype are associated with metabolic risk factors.</pubmed_title><pmcid>PMC3004038</pmcid><funding_grant_id>GR079534</funding_grant_id><funding_grant_id>G0700342</funding_grant_id><funding_grant_id>K2010-55X-11285-13</funding_grant_id><funding_grant_id>K2009-65X-15424-05</funding_grant_id><pubmed_authors>Walley A</pubmed_authors><pubmed_authors>Thelle DS</pubmed_authors><pubmed_authors>Carlsson LM</pubmed_authors><pubmed_authors>Jacobson P</pubmed_authors><pubmed_authors>Olsson M</pubmed_authors><pubmed_authors>Froguel P</pubmed_authors><pubmed_authors>Sjoholm K</pubmed_authors><pubmed_authors>Olsson B</pubmed_authors><pubmed_authors>Bjorkegren J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Expression of the selenoprotein S (SELS) gene in subcutaneous adipose tissue and SELS genotype are associated with metabolic risk factors.</name><description>The selenoprotein S (SELS) is a putative receptor for serum amyloid A, and recent studies have suggested that SELS may be a link between type 2 diabetes mellitus and inflammation. Genetic studies of SELS polymorphisms have revealed associations with circulating levels of inflammatory markers and hard end points of cardiovascular disease. In this study, we analyzed SELS expression in subcutaneous adipose tissue and SELS genotype in relation to metabolic risk factors. DNA microarray expression analysis was used to study the expression of SELS in lean and obese siblings from the Swedish Obese Subjects Sib Pair Study. TaqMan genotyping was used to analyze 3 polymorphisms, previously found to be associated with circulating levels of inflammatory markers, in the INTERGENE case-control study of m</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Jan</publication><modification>2026-05-03T06:33:44.637Z</modification><creation>2026-04-07T18:56:11.274Z</creation></dates><accession>S-EPMC3004038</accession><cross_references><pubmed>20619427</pubmed><doi>10.1016/j.metabol.2010.05.011</doi></cross_references></HashMap>