title: Influence of obesity and insulin sensitivity on phospholipid transfer protein activity.
abstract: OBJECTIVE
  Phospholipid transfer protein plays a key role in lipoprotein metabolism by catalysing the transfer of phospholipids from triglyceride-rich lipoproteins to high-density lipoproteins and, also, within the high-density lipoprotein family, from particle to particle. This transfer results in a change of HDL particle size and the generation of pre-beta-high-density lipoproteins which function as initial lipid acceptors in the process of reverse cholesterol transport. Because adipose tissue is a source of phospholipid transfer protein we investigated the influence of obesity and insulin sensitivity on phospholipid transfer protein activity.
  
  
  METHODS
  Using an exogenous substrate assay phospholipid transfer protein activity was measured in plasma specimens of 190 normolipidaemic, non-diabetic subjects with BMI ranging from 19 to 43 kg/m2. Insulin sensitivity was measured by the short insulin tolerance test.
  
  
  RESULTS
  Phospholipid transfer protein activity was associated with BMI (r = 0.46, p < 0.01), body fat mass (r = 0.39, p < 0.01), subcutaneous fat area (r = 0.32, p < 0.01) and plasma leptin concentration (r = 0.24, p < 0.01) but not with insulin sensitivity expressed as the k(s) of the insulin tolerance test (kITT value) (r = -0.14, p = 0.40). Accordingly, phospholipid transfer protein activity was higher in obese than in nonobese subjects. As determined by linear regression analysis, BMI was the sole predictor of phospholipid transfer protein activity in plasma explaining 22.2% of the activity (p< 0.01).
  
  
  CONCLUSIONS
  This data suggests that increased phospholipid transfer protein activity in obese subjects is a consequence of obesity itself without the contribution of insulin resistance and can be explained by increased synthesis of phospholipid transfer protein from the enlarged mass of adipose tissue.
authors.affiliation: Department of Internal Medicine, University of Innsbruck, Austria.
authors.forename: S
authors.initials: S
authors.lastname: Kaser
authors.forename: A
authors.initials: A
authors.lastname: Sandhofer
authors.forename: B
authors.initials: B
authors.lastname: Föger
authors.forename: C F
authors.initials: CF
authors.lastname: Ebenbichler
authors.forename: B
authors.initials: B
authors.lastname: Igelseder
authors.forename: L
authors.initials: L
authors.lastname: Malaimare
authors.forename: B
authors.initials: B
authors.lastname: Paulweber
authors.forename: J R
authors.initials: JR
authors.lastname: Patsch
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D000368:Aged; D001823:Body Composition; D015992:Body Mass Index; D002352:Carrier Proteins / Q000097:blood*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007328:Insulin; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D016014:Linear Models; D008297:Male; D008565:Membrane Proteins / Q000097:blood*; D008875:Middle Aged; D009765:Obesity / Q000097:blood*; D049294:Phospholipid Transfer Proteins
chemical_list: D002352:Carrier Proteins; D006442:Glycated Hemoglobin; D007328:Insulin; D020738:Leptin; D008565:Membrane Proteins; D049294:Phospholipid Transfer Proteins