Influence of obesity and insulin sensitivity on phospholipid transfer protein activity

Aims/hypothesis. Phospholipid transfer protein plays a key role in lipoprot ein metabolism by catalysing the transfer of phospholipids from triglycerid e-rich lipoproteins to high-density lipoproteins and, also, within the high -density lipoprotein family, from particle to particle. This transfer resul ts in a change of HDL particle size and the generation of pre-beta -high-de nsity lipoproteins which function as initial lipid acceptors in the process of reverse cholesterol transport. Because adipose tissue is a source of ph ospholipid transfer protein we investigated the influence of obesity and in sulin sensitivity on phospholipid transfer protein activity. Methods. Using an exogenous substrate assay phospholipid transfer protein activity was me asured in plasma specimens of 190 normolipidaemic, non-diabetic betic subje cts with BMI ranging from 19 to 43 kg/m(2). Insulin sensitivity was measure d by the short insulin tolerance test. (r = 0.39, p < 0.01), subcutaneous f at 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 insuli n tolerance test (kITT value) (r = -0.14, p = 0.40). Accordingly, phospholi pid transfer protein activity was higher in obese than in nonobese subjects . As determined by linear regression analysis, BMI was the sole predictor o f phospholipid transfer protein activity in plasma explaining 22.2 % of the activity (p<less than> 0.01). Results. Phospholipid transfer protein activ ity 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 conc entration (r = 0.24, p < 0.01) but not with insulin sensitivity expressed a s 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/interpretations. This data suggests that increased phospholipid transfer protein activity i n obese subjects is a consequence of obesity itself without the contributio n of insulin resistance and can be explained by increased synthesis of phos pholipid transfer protein from the enlarged mass of adipose tissue.