OBJECTIVES: The high density lipoprotein Anionic Peptide Factor (HDL(3)-APF) was previously described as an apolipoprotein that promotes the reverse cholesterol transport. Since phospholipid transfer protein (PLTP) is involved in such mechanism we attempted to focus on the two APF and PLTP proteins. DESIGN AND METHODS: We recruited 56 type 2 diabetic patients with (n=36) or without (n=20) coronary artery disease (CAD) and 19 CAD patients. The three groups were compared to 39 healthy control subjects. In all groups, lipid profile was determined and plasma APF concentrations and PLTP activity were measured. RESULTS: In all patients, the PLTP activity was significantly increased in comparison with controls (p<0.01), in concomitance with a plasma APF level decrease in groups with CAD (with and without type 2 diabetes) (p<0.01). Multiple linear regression analysis demonstrated that, when apoA-I, HDL-C, HDL-phospholipids and PLTP activity were taken into account as independent variables (after univariate regression analysis), HDL-PL was positively and independently related to APF (p<0.0001 in whole population; p=0.0090 in controls) and PLTP activity was negatively and independently related to APF in whole population and all patients' groups (all p<0.05), but positively and independently associated to APF in controls (p=0.0005). CONCLUSIONS: APF could be considered as a specific marker against CAD and type 2 diabetes mellitus and our results confirm the atherogenic behavior of PLTP in CAD. Thus, these two proteins are likely to be regulated in a reverse manner.
OBJECTIVES: The high density lipoprotein Anionic Peptide Factor (HDL(3)-APF) was previously described as an apolipoprotein that promotes the reverse cholesterol transport. Since phospholipid transfer protein (PLTP) is involved in such mechanism we attempted to focus on the two APF and PLTP proteins. DESIGN AND METHODS: We recruited 56 type 2 diabeticpatients with (n=36) or without (n=20) coronary artery disease (CAD) and 19 CAD patients. The three groups were compared to 39 healthy control subjects. In all groups, lipid profile was determined and plasma APF concentrations and PLTP activity were measured. RESULTS: In all patients, the PLTP activity was significantly increased in comparison with controls (p<0.01), in concomitance with a plasma APF level decrease in groups with CAD (with and without type 2 diabetes) (p<0.01). Multiple linear regression analysis demonstrated that, when apoA-I, HDL-C, HDL-phospholipids and PLTP activity were taken into account as independent variables (after univariate regression analysis), HDL-PL was positively and independently related to APF (p<0.0001 in whole population; p=0.0090 in controls) and PLTP activity was negatively and independently related to APF in whole population and all patients' groups (all p<0.05), but positively and independently associated to APF in controls (p=0.0005). CONCLUSIONS: APF could be considered as a specific marker against CAD and type 2 diabetes mellitus and our results confirm the atherogenic behavior of PLTP in CAD. Thus, these two proteins are likely to be regulated in a reverse manner.