title: Reduced adipose tissue inflammation represents an intermediate cardiometabolic phenotype in obesity.
abstract: OBJECTIVE
  The purpose of this study was to determine whether obese individuals with reduced adipose tissue inflammation exhibit a more favorable cardiovascular risk profile.
  
  
  BACKGROUND
  Obesity is associated with a low-grade state of chronic inflammation that might be causally related to cardiometabolic disease.
  
  
  METHODS
  With immunohistochemistry, we categorized obese individuals dichotomously as having inflamed fat (n = 78) or noninflamed fat (n = 31) on the basis of the presence (+) or absence (-) of macrophage crown-like structures (CLS) in subcutaneous abdominal fat biopsy samples. We compared their metabolic, vascular, and adipose tissue characteristics with lean subjects (n = 17).
  
  
  RESULTS
  Inflamed CLS+ obese individuals displayed higher plasma insulin, homeostasis model assessment, triglycerides, glucose, blood pressure, high-sensitivity C-reactive protein, low-density lipoprotein cholesterol, lower high-density lipoprotein cholesterol, and brachial artery flow-mediated dilation compared with lean subjects (p < 0.05). Adipose messenger ribonucleic acid expression of inflammatory genes including CD68, leptin, matrix metalloproteinase-9, CD163, and CD8A were significantly greater and vascular endothelial growth factor was lower in the CLS+ group (p < 0.05). In contrast, obese subjects with noninflamed fat exhibited a mixed clinical phenotype with lower insulin resistance, reduced proatherogenic gene expression, and preserved vascular function as in lean subjects. In multiple linear regression adjusting for age and sex, CLS status (beta = -0.28, p = 0.008) and waist circumference (beta = -0.25, p = 0.03) were independent predictors of flow-mediated dilation.
  
  
  CONCLUSIONS
  These findings lend support to the novel concept that factors in addition to absolute weight burden, such as qualitative features of adipose tissue, might be important determinants of cardiovascular disease. Therapeutic modulation of the adipose phenotype might represent a target for treatment in obesity.
authors: Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.
authors: Melissa G
authors: MG
authors: Farb
authors: Sherman
authors: S
authors: Bigornia
authors: Melanie
authors: M
authors: Mott
authors: Kahraman
authors: K
authors: Tanriverdi
authors: Kristine M
authors: KM
authors: Morin
authors: Jane E
authors: JE
authors: Freedman
authors: Lija
authors: L
authors: Joseph
authors: Donald T
authors: DT
authors: Hess
authors: Caroline M
authors: CM
authors: Apovian
authors: Joseph A
authors: JA
authors: Vita
authors: Noyan
authors: N
authors: Gokce
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D015992:Body Mass Index; D001916:Brachial Artery / Q000503:physiopathology; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D002784:Cholesterol / Q000097:blood; D005260:Female; D006801:Humans; D007249:Inflammation; D007328:Insulin / Q000097:blood; D008264:Macrophages / Q000473:pathology; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000150:complications; D009765:Obesity / Q000097:blood* / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D050177:Overweight / Q000473:pathology; D010641:Phenotype; D050507:Subcutaneous Fat, Abdominal / Q000473:pathology*; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D002097:C-Reactive Protein; D002784:Cholesterol