Diabetologia

, Volume 44, Issue 9, pp 1111-1117

Influence of obesity and insulin sensitivity on phospholipid transfer protein activity

  • S. KaserAffiliated withDepartment of Internal Medicine, University of Innsbruck, Innsbruck, Austria
  • , A. SandhoferAffiliated withDepartment of Internal Medicine, University of Innsbruck, Innsbruck, Austria
  • , B. FögerAffiliated withDepartment of Internal Medicine, University of Innsbruck, Innsbruck, Austria
  • , C. F. EbenbichlerAffiliated withDepartment of Internal Medicine, University of Innsbruck, Innsbruck, Austria
  • , B. IgelsederAffiliated withDepartment of Neurology, Christian Doppler Klinik, Salzburg, Austria
  • , L. MalaimareAffiliated withFirst Department of Internal Medicine, General Hospital Salzburg, Salzburg, Austria
  • , B. PaulweberAffiliated withFirst Department of Internal Medicine, General Hospital Salzburg, Salzburg, Austria
  • , J. R. PatschAffiliated withDepartment of Internal Medicine, University of Innsbruck, Innsbruck, Austria

Abstract.

Aims/hypothesis:

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-β-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 ks of the insulin tolerance test (kITT value) (r = –0.14, p = 0.40). Accordingly, phospholipid transfer protein activity was higher in obese than in non-obese 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/interpretations:

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. [Diabetologia (2001) 44: 1111–1117]

Keywords Phospholipid transfer protein, obesity, insulin sensitivity, adipose tissue, body mass index.