title: Adipose tissue dysregulation in patients with metabolic syndrome.
abstract: BACKGROUND
  The metabolic syndrome (MetS) is associated with increased risk of diabetes and cardiovascular disease (CVD). Numerous groups have shown increased circulating biomarkers of inflammation in MetS. However, there are scanty data on the cellular sources contributing to this low-grade inflammation.
  
  
  OBJECTIVE
  The aim of this study was to determine the role of sc adipose tissue (SAT) biology in nascent MetS without concomitant diabetes or CVD.
  
  
  METHODS
  Subjects with MetS and controls were recruited after informed consent. Fasting blood was collected, and SAT was obtained by biopsy.
  
  
  RESULTS
  Circulating biomarkers of inflammation and insulin resistance, high-sensitivity C-reactive protein (hsCRP), IL-6, IL-1β, leptin, serum amyloid A, and retinol-binding protein-4 (RBP-4) concentrations were significantly higher in the MetS subjects than controls, whereas adiponectin concentrations were lower. In SAT, leptin, RBP-4, CRP, serum amyloid A, plasminogen activator inhibitor-1, IL-1, IL-6, IL-8, and monocyte chemotactic protein-1 (MCP-1) levels were significantly higher in MetS than controls. These differences except for RBP-4 persisted after adjusting for waist circumference. In addition, there were significantly increased numbers of macrophages infiltrating the SAT of MetS and increased numbers of crown-like structures compared with controls. hsCRP correlated positively with homeostasis model assessment and SAT MCP-1 and negatively with adiponectin. Homeostasis model assessment correlated positively with plasminogen activator inhibitor-1, RBP-4, and SAT MCP-1.
  
  
  CONCLUSIONS
  We make the novel observation that SAT of MetS has increased macrophage recruitment with cardinal crown-like structure features and contributes to the increased cellular inflammation that produces increased levels of biomarkers that are correlated with both insulin resistance and low-grade inflammation. These aberrations could contribute to the progression of MetS and the increased risk for diabetes and CVD.
authors.affiliation: Department of Pediatrics, Vanderbilt University, Nashville, Tennessee 37232, USA.
authors.forename: Andrew A
authors.initials: AA
authors.lastname: Bremer
authors.forename: Sridevi
authors.initials: S
authors.lastname: Devaraj
authors.forename: Alaa
authors.initials: A
authors.lastname: Afify
authors.forename: Ishwarlal
authors.initials: I
authors.lastname: Jialal
mesh_terms: D052242:Adiponectin / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism / Q000503:physiopathology*; D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D020738:Leptin / Q000378:metabolism; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism / Q000503:physiopathology*; D008875:Middle Aged; D055105:Waist Circumference
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D018925:Chemokines; D016207:Cytokines; D020738:Leptin; D002097:C-Reactive Protein