title: Association of adipocyte genes with ASP expression: a microarray analysis of subcutaneous and omental adipose tissue in morbidly obese subjects.
abstract: BACKGROUND
  Prevalence of obesity is increasing to pandemic proportions. However, obese subjects differ in insulin resistance, adipokine production and co-morbidities. Based on fasting plasma analysis, obese subjects were grouped as Low Acylation Stimulating protein (ASP) and Triglyceride (TG) (LAT) vs High ASP and TG (HAT). Subcutaneous (SC) and omental (OM) adipose tissues (n = 21) were analysed by microarray, and biologic pathways in lipid metabolism and inflammation were specifically examined.
  
  
  METHODS
  LAT and HAT groups were matched in age, obesity, insulin, and glucose, and had similar expression of insulin-related genes (InsR, IRS-1). ASP related genes tended to be increased in the HAT group and were correlated (factor B, adipsin, complement C3, p < 0.01 each). Differences between LAT and HAT group were almost exclusively in SC tissue, with little difference in OM tissue. Increased C5L2 (p < 0.01), an ASP receptor, in HAT suggests a compensatory ASP pathway, associated with increased TG storage.
  
  
  RESULTS
  HAT adipose tissue demonstrated increased lipid related genes for storage (CD36, DGAT1, DGAT2, SCD1, FASN, and LPL), lipolysis (HSL, CES1, perilipin), fatty acid binding proteins (FABP1, FABP3) and adipocyte differentiation markers (CEBPalpha, CEBPbeta, PPARgamma). By contrast, oxidation related genes were decreased (AMPK, UCP1, CPT1, FABP7). HAT subjects had increased anti-inflammatory genes TGFB1, TIMP1, TIMP3, and TIMP4 while proinflammatory PIG7 and MMP2 were also significantly increased; all genes, p < 0.025.
  
  
  CONCLUSIONS
  Taken together, the profile of C5L2 receptor, ASP gene expression and metabolic factors in adipose tissue from morbidly obese HAT subjects suggests a compensatory response associated with the increased plasma ASP and TG.
authors.affiliation: Centre de Recherche Institut Universitaire de Cardiologie et de Pneumologie de Quebec, Laval University, Quebec, Canada.
authors.forename: Robin E
authors.initials: RE
authors.lastname: MacLaren
authors.forename: Wei
authors.initials: W
authors.lastname: Cui
authors.forename: HuiLing
authors.initials: H
authors.lastname: Lu
authors.forename: Serge
authors.initials: S
authors.lastname: Simard
authors.forename: Katherine
authors.initials: K
authors.lastname: Cianflone
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology / Q000378:metabolism*; D000328:Adult; D003176:Complement C3; D050556:Fatty Acid-Binding Proteins / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000235:genetics; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D050356:Lipid Metabolism / Q000235:genetics; D008297:Male; D046228:Microarray Analysis; D008875:Middle Aged; D009765:Obesity / Q000235:genetics*; D009852:Omentum / Q000033:anatomy & histology; D044087:Receptor, Anaphylatoxin C5a; D019707:Receptors, Chemokine / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050151:Subcutaneous Fat / Q000033:anatomy & histology / Q000378:metabolism*; D014280:Triglycerides / Q000097:blood
chemical_list: C038245:C3 protein, human; C417003:C5aR2 protein, human; D003176:Complement C3; D050556:Fatty Acid-Binding Proteins; D036341:Intercellular Signaling Peptides and Proteins; D044087:Receptor, Anaphylatoxin C5a; D019707:Receptors, Chemokine; D014280:Triglycerides