title: Increased chemerin and decreased omentin-1 in both adipose tissue and plasma in nascent metabolic syndrome.
abstract: BACKGROUND
  Adipose tissue dysregulation causing aberrant adipokine secretion contributes toward the proinflammatory state of metabolic syndrome (MetS). However, there are scant data on the role of novel adipokines in MetS.
  
  
  OBJECTIVE
  The aim of this study was to determine the levels of circulating and adipose tissue-secreted adipokines, chemerin, omentin-1, resistin, and visfatin in nascent MetS patients without diabetes or cardiovascular disease and to determine their relation with features of MetS.
  
  
  METHODS
  Subjects with MetS and gender- and age-matched controls were recruited after informed consent. Fasting blood samples and gluteal subcutaneous adipose tissue (SAT) biopsies were obtained.
  
  
  RESULTS
  SAT-secreted and plasma levels of chemerin, omentin-1, resistin, and visfatin were quantitated.
  
  
  RESULTS
  There was significantly higher circulating as well as SAT-released chemerin in nascent MetS compared to controls, which persisted after adjustment for body mass index, waist circumference, and age. Also, both SAT-released and plasma levels of omentin-1 were significantly lower in MetS compared to controls, and the significant differences persisted after adjustment for age, body mass index, or waist circumference. No significant differences were observed in the levels of circulating visfatin as well as SAT-secreted resistin and visfatin. Chemerin correlated significantly with high-sensitivity C-reactive protein, homeostasis model of assessment for insulin resistance, triglycerides, and blood pressure, and inversely with omentin and high-density lipoprotein cholesterol. Omentin correlated significantly with high-density lipoprotein cholesterol and inversely with glucose and triglycerides.
  
  
  CONCLUSIONS
  We make the novel observation of abnormal circulating and gluteal SAT-secreted chemerin and omentin-1 levels in nascent MetS, which could confer a higher risk for diabetes and cardiovascular disease.
authors.affiliation: Laboratory of Atherosclerosis and Metabolic Research, Department of Pathology and Laboratory Medicine, University of California at Davis, Sacramento, California 95817, USA. ishwarlal.jialal@ucdmc.ucdavis.edu
authors.forename: Ishwarlal
authors.initials: I
authors.lastname: Jialal
authors.forename: Sridevi
authors.initials: S
authors.lastname: Devaraj
authors.forename: Harmeet
authors.initials: H
authors.lastname: Kaur
authors.forename: Beverley
authors.initials: B
authors.lastname: Adams-Huet
authors.forename: Andrew A
authors.initials: AA
authors.lastname: Bremer
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000378:metabolism; D018925:Chemokines / Q000097:blood / Q000378:metabolism*; D016207:Cytokines / Q000097:blood / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000378:metabolism; D005260:Female; D058851:GPI-Linked Proteins / Q000097:blood / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000502:physiology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D037102:Lectins / Q000097:blood / Q000378:metabolism*; D008055:Lipids / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000453:epidemiology / Q000378:metabolism*; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood / Q000378:metabolism; D052243:Resistin / Q000097:blood / Q000378:metabolism; D012307:Risk Factors; D050151:Subcutaneous Fat / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D018925:Chemokines; D016207:Cytokines; D058851:GPI-Linked Proteins; C432397:ITLN1 protein, human; D036341:Intercellular Signaling Peptides and Proteins; D037102:Lectins; D008055:Lipids; C478630:RARRES2 protein, human; C499624:RETN protein, human; D052243:Resistin; D051547:Heme Oxygenase-1; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human