title: Regional impact of adipose tissue morphology on the metabolic profile in morbid obesity.
abstract: OBJECTIVE
  The aim of this study was to determine whether the mean size of fat cells in either visceral or subcutaneous adipose tissue has an impact on the metabolic and inflammatory profiles in morbid obesity.
  
  
  METHODS
  In 80 morbidly obese women, mean visceral (omental) and subcutaneous fat cell sizes were related to in vivo markers of inflammation, glucose metabolism and lipid metabolism.
  
  
  RESULTS
  Visceral, but not subcutaneous, adipocyte size was significantly associated with plasma apolipoprotein B, total cholesterol, LDL-cholesterol and triacylglycerols (p ranging from 0.002 to 0.015, partial r ranging from 0.3 to 0.4). Subcutaneous, but not visceral, adipocyte size was significantly associated with plasma insulin and glucose, insulin-induced glucose disposal and insulin sensitivity (p ranging from 0.002 to 0.005, partial r ranging from -0.34 to 0.35). The associations were independent of age, BMI, body fat mass or body fat distribution. Adipose tissue hyperplasia (i.e. many small adipocytes) in both regions was significantly associated with better glucose, insulin and lipid profiles compared with adipose hypertrophy (i.e. few large adipocytes) in any or both regions (p ranging from <0.0001 to 0.04). Circulating inflammatory markers were not associated with fat cell size or corresponding gene expression in the fat cell regions examined.
  
  
  CONCLUSIONS
  In morbidly obese women region-specific variations in mean adipocyte size are associated with metabolic complications but not systemic or adipose inflammation. Large fat cells in the visceral region are linked to dyslipidaemia, whereas large subcutaneous adipocytes are important for glucose and insulin abnormalities. Hyperplasia (many small adipocytes) in both adipose regions may be protective against lipid as well as glucose/insulin abnormalities in obesity.
authors.affiliation: Department of Medicine, Karolinska Institute at Karolinska Hospital, Huddinge, CME, SE-141 86 Stockholm, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Hoffstedt
authors.forename: E
authors.initials: E
authors.lastname: Arner
authors.forename: H
authors.initials: H
authors.lastname: Wahrenberg
authors.forename: D P
authors.initials: DP
authors.lastname: Andersson
authors.forename: V
authors.initials: V
authors.lastname: Qvisth
authors.forename: P
authors.initials: P
authors.lastname: Löfgren
authors.forename: M
authors.initials: M
authors.lastname: Rydén
authors.forename: A
authors.initials: A
authors.lastname: Thörne
authors.forename: M
authors.initials: M
authors.lastname: Wirén
authors.forename: M
authors.initials: M
authors.lastname: Palmér
authors.forename: A
authors.initials: A
authors.lastname: Thorell
authors.forename: E
authors.initials: E
authors.lastname: Toft
authors.forename: P
authors.initials: P
authors.lastname: Arner
mesh_terms: D017667:Adipocytes / Q000473:pathology; D000273:Adipose Tissue / Q000473:pathology* / Q000502:physiology; D000328:Adult; D001055:Apolipoproteins B / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D048429:Cell Size; D005260:Female; D015309:Glucose Clamp Technique; D006801:Humans; D007328:Insulin / Q000097:blood; D050152:Intra-Abdominal Fat / Q000378:metabolism / Q000473:pathology; D055442:Metabolome / Q000502:physiology*; D008875:Middle Aged; D009767:Obesity, Morbid / Q000378:metabolism* / Q000473:pathology*; D050151:Subcutaneous Fat / Q000378:metabolism / Q000473:pathology; D014280:Triglycerides / Q000097:blood; D055815:Young Adult
chemical_list: D001055:Apolipoproteins B; D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides