title: Insulin resistance is associated with a modest increase in inflammation in subcutaneous adipose tissue of moderately obese women.
abstract: OBJECTIVE
  We have previously described differences in adipose cell size distribution and expression of genes related to adipocyte differentiation in subcutaneous abdominal fat obtained from insulin-sensitive (IS) and -resistant (IR) persons, matched for degree of moderate obesity. To determine whether other biological properties also differ between IR and IS obese individuals, we quantified markers of inflammatory activity in adipose tissue from overweight IR and IS individuals.
  
  
  METHODS
  Subcutaneous abdominal tissue was obtained from moderately obese women, divided into IR (n = 14) and IS (n = 19) subgroups by determining their steady-state plasma glucose (SSPG) concentrations during the insulin suppression test. Inflammatory activity was assessed by comparing expression of nine relevant genes and by immunohistochemical quantification of CD45- and CD68-containing cells.
  
  
  RESULTS
  SSPG concentrations were approximately threefold higher in IR than in IS individuals. Expression levels of CD68, EMR1, IL8, IL6 and MCP/CCL2 mRNAs were modestly but significantly increased (p < 0.05) in IR compared with IS participants. Results of immunohistochemical staining were consistent with gene expression data, demonstrating modest differences between IR and IS individuals. Crown-like structures, in which macrophages surround single adipocytes, were rarely seen in tissue from either subgroup.
  
  
  CONCLUSIONS
  A modest increase in inflammatory activity was seen in subcutaneous adipose tissue from IR compared with equally obese IS individuals. Together with previous evidence of impaired adipose cell differentiation in IR vs equally obese individuals, it appears that at least two biological processes in subcutaneous adipose tissue characterize the insulin-resistant state independent of obesity per se.
authors.affiliation: Department of Medicine, Division of Endocrinology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305-5103, USA. tmclaugh@stanford.edu
authors.forename: T
authors.initials: T
authors.lastname: McLaughlin
authors.forename: A
authors.initials: A
authors.lastname: Deng
authors.forename: O
authors.initials: O
authors.lastname: Gonzales
authors.forename: M
authors.initials: M
authors.lastname: Aillaud
authors.forename: G
authors.initials: G
authors.lastname: Yee
authors.forename: C
authors.initials: C
authors.lastname: Lamendola
authors.forename: F
authors.initials: F
authors.lastname: Abbasi
authors.forename: A J
authors.initials: AJ
authors.lastname: Connolly
authors.forename: A
authors.initials: A
authors.lastname: Sherman
authors.forename: S W
authors.initials: SW
authors.lastname: Cushman
authors.forename: G
authors.initials: G
authors.lastname: Reaven
authors.forename: P S
authors.initials: PS
authors.lastname: Tsao
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D007333:Insulin Resistance; D017493:Leukocyte Common Antigens / Q000378:metabolism; D008875:Middle Aged; D009765:Obesity / Q000235:genetics / Q000378:metabolism*; D050151:Subcutaneous Fat / Q000378:metabolism*
chemical_list: D018836:Inflammation Mediators; D017493:Leukocyte Common Antigens