title: Subcutaneous adipose tissue expression of plasminogen activator inhibitor-1 (PAI-1) in nondiabetic and Type 2 diabetic subjects.
abstract: OBJECTIVE
  Increased plasma levels of plasminogen activator inhibitor-1 (PAI-1) have been suggested to be a part of the insulin resistance syndrome, and recent data suggest that adipose tissue participates in the production of PAI-1. We examined the expression and insulin regulation of subcutaneous adipose tissue PAI-1 mRNA and its relationship to insulin sensitivity.
  
  
  METHODS
  A cross-sectional study involving five lean (60.0+/-3.1 years, BMI 23.5+/-0.5 kg/m(2)) and six obese nondiabetic men (56.0+/-3.1 years, BMI 30.4+/-0.7 kg/m(2)), and six obese Type 2 diabetic men (61.4+/-3.2 years, BMI 31.8+/-1.0 kg/m(2)).
  
  
  METHODS
  Subcutaneous adipose tissue PAI-1 mRNA and insulin sensitivity were quantified using RT-competitive PCR and euglycemic hyperinsulinemic clamp technique, respectively.
  
  
  RESULTS
  Subcutaneous adipose tissue PAI-1 mRNA levels were higher in obese nondiabetic and Type 2 diabetic men than in lean nondiabetic men. PAI-1 mRNA levels decreased in the three groups during a 240-min euglycemic hyperinsulinemic clamp (P<0.05 for all groups), and a similar reduction was observed during a 240-min saline control study indicating that adipose tissue PAI-1 gene expression has diurnal variation and is not acutely controlled by hyperinsulinemia. The basal PAI-1 mRNA levels correlated positively with BMI, and waist-to-hip ratio; and negatively with whole-body glucose disposal rate in nondiabetic men.
  
  
  CONCLUSIONS
  Subcutaneous adipose tissue PAI-1 mRNA expression is increased in obese nondiabetic or in Type 2 diabetic men. Subcutaneous adipose tissue PAI-1 mRNA expression is increased in proportion to visceral obesity and to the level of whole-body insulin resistance. Subcutaneous adipose tissue PAI-1 mRNA expression is not acutely regulated by insulin, and it is subject to a diurnal variation.
authors.affiliation: Department of Medicine, Division of Geriatrics, Helsinki University Central Hospital, Helsinki, Finland. heikki_koistinen@yahoo.com
authors.forename: H A
authors.initials: HA
authors.lastname: Koistinen
authors.forename: E
authors.initials: E
authors.lastname: Dusserre
authors.forename: P
authors.initials: P
authors.lastname: Ebeling
authors.forename: P
authors.initials: P
authors.lastname: Vallier
authors.forename: V A
authors.initials: VA
authors.lastname: Koivisto
authors.forename: H
authors.initials: H
authors.lastname: Vidal
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D003430:Cross-Sectional Studies; D003920:Diabetes Mellitus / Q000235:genetics* / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics* / Q000503:physiopathology; D015309:Glucose Clamp Technique; D006801:Humans; D006946:Hyperinsulinism; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000235:genetics* / Q000503:physiopathology; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D012333:RNA, Messenger / Q000032:analysis; D012016:Reference Values; D012867:Skin; D014158:Transcription, Genetic
chemical_list: D001786:Blood Glucose; D017395:Plasminogen Activator Inhibitor 1; D012333:RNA, Messenger