title: Macrophages and fibrosis in adipose tissue are linked to liver damage and metabolic risk in obese children.
abstract: OBJECTIVE
  Obesity in childhood is associated with an inflammatory state in adipose tissue and liver, which elevates risk for diabetes and liver disease. No prior study has examined associations between pathologies occurring in adipose tissue and liver to identify elements of tissue damage associated with type 2 diabetes risk. This study sought to determine whether inflammation and fibrosis in abdominal subcutaneous adipose tissue (SAT) in obese/overweight children (BMI-z 2.3 ± 0.76) was related to the extent of observed liver disease or type 2 diabetes risk.
  
  
  METHODS
  Biopsy samples of abdominal (SAT) and liver were simultaneously collected from 33 Italian children (mean BMI 28.1 ± 5.1 kg/m(2) and mean age 11.6 ± 2.2 years) with confirmed NAFLD. Histology and immunohistochemistry were conducted on biopsies to assess inflammation and fibrosis in adipose tissue and fibrosis and inflammation in liver.
  
  
  RESULTS
  Presence vs. absence of crown-like structures (CLS) in SAT was significantly related to liver fibrosis scores (1.7 ± 0.7 vs. 1.2 ± 0.7, P = 0.04) independent of BMI. SAT fibrosis was significantly correlated with a lower disposition index (r = -0.48, P = 0.006). No other adipose measures were associated with liver disease parameters.
  
  
  CONCLUSIONS
  Markers of subcutaneous white adipose tissue inflammation are associated with greater extent of liver fibrosis independent of obesity and SAT fibrosis may contribute to diabetes risk through reduced insulin secretion.
authors.affiliation: Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine, Mount Sinai, New York, USA.
authors.forename: Ryan W
authors.initials: RW
authors.lastname: Walker
authors.forename: Hooman
authors.initials: H
authors.lastname: Allayee
authors.forename: Alessandro
authors.initials: A
authors.lastname: Inserra
authors.forename: Rodolfo
authors.initials: R
authors.lastname: Fruhwirth
authors.forename: Anna
authors.initials: A
authors.lastname: Alisi
authors.forename: Rita
authors.initials: R
authors.lastname: Devito
authors.forename: Magalie E
authors.initials: ME
authors.lastname: Carey
authors.forename: Frank
authors.initials: F
authors.lastname: Sinatra
authors.forename: Michael I
authors.initials: MI
authors.lastname: Goran
authors.forename: Valerio
authors.initials: V
authors.lastname: Nobili
mesh_terms: D052242:Adiponectin / Q000097:blood; D050154:Adiposity; D000293:Adolescent; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001827:Body Height; D015992:Body Mass Index; D001835:Body Weight; D002097:C-Reactive Protein / Q000378:metabolism; D002648:Child; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism; D005215:Fasting; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D050152:Intra-Abdominal Fat / Q000473:pathology*; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000150:complications / Q000473:pathology*; D008264:Macrophages / Q000166:cytology*; D008297:Male; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D011446:Prospective Studies; D012307:Risk Factors; D050507:Subcutaneous Fat, Abdominal / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase