title: Serum phospholipid transfer protein activity after a high fat meal in patients with insulin-treated type 2 diabetes.
abstract: Plasma phospholipid transfer protein (PLTP) mediates both net transfer and exchange of phospholipids between different lipoproteins. Animal studies have shown that it is closely related to the development of atherosclerosis. Although many studies have indicated that PLTP activity is increased in diabetes mellitus, the role of PLTP in diabetes is still unclear. To evaluate the influence of a high-fat meal on PLTP activity, 50 nondiabetic patients with coronary heart disease (CHD), 50 insulin-treated Type 2 diabetics, and 50 healthy controls were included. We determined PLTP activity before and 4 and 8 h after a high-fat meal. As expected, serum PLTP activity was significantly higher in CHD patients than in healthy controls (71.0 +/- 46.2 vs. 54.0 +/- 33.8 pmol/microl/h, P = 0.032) at baseline. More importantly, we found that serum PLTP activity increased to its maximum 4 h after fat loading and then decreased to nearly basal levels after 8 h both in controls and CHD patients. In contrast, PLTP activity continuously increased during this time period in the diabetic patients. With regards to the data from this study we hypothesize that serum PLTP is involved in the clearance of postprandial lipoproteins and this process is attenuated in diabetes. Since postprandial lipoproteins are atherogenic, the delay in clearance of these particles could play an important role in the development of atherosclerosis in patients with diabetes mellitus.
authors.affiliation: Department of Medicine III, Martin Luther-University, Halle, Germany. axel.schlitt@medizin.uni-halle.de
authors.forename: Axel
authors.initials: A
authors.lastname: Schlitt
authors.forename: Bernhard
authors.initials: B
authors.lastname: Schwaab
authors.forename: Kirsten
authors.initials: K
authors.lastname: Fingscheidt
authors.forename: Karl J
authors.initials: KJ
authors.lastname: Lackner
authors.forename: Gunnar H
authors.initials: GH
authors.lastname: Heine
authors.forename: Alexander
authors.initials: A
authors.lastname: Vogt
authors.forename: Michael
authors.initials: M
authors.lastname: Buerke
authors.forename: Lars
authors.initials: L
authors.lastname: Maegdefessel
authors.forename: Uwe
authors.initials: U
authors.lastname: Raaz
authors.forename: Karl
authors.initials: K
authors.lastname: Werdan
authors.forename: Xian-Cheng
authors.initials: XC
authors.lastname: Jiang
mesh_terms: D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000209:etiology; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D004041:Dietary Fats / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D049294:Phospholipid Transfer Proteins / Q000097:blood*; D011446:Prospective Studies; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D004041:Dietary Fats; D007328:Insulin; D049294:Phospholipid Transfer Proteins; D014280:Triglycerides; D002097:C-Reactive Protein; D002784:Cholesterol