title: Acute and chronic effects of a 24-hour intravenous triglyceride emulsion challenge on plasma lecithin: cholesterol acyltransferase, phospholipid transfer protein, and cholesteryl ester transfer protein activities.
abstract: Lecithin:cholesterol acyltransferase (LCAT), phospholipid transfer protein (PLTP), and cholesteryl ester transfer protein (CETP) are key factors in remodeling of high density lipoproteins (HDL) and triglyceride-rich lipoproteins. We examined the effect of a large, 24 h intravenous fat load on plasma lipids and free fatty acids (FFA) as well as on plasma LCAT, PLTP, and CETP activity levels in 8 healthy men. The effect of concomitant insulin infusion was also studied, with 1 week between the study days. During Lipofundin(R) infusion, plasma triglycerides and FFA strongly increased after 8 and 24 h (P < 0.001), whereas HDL cholesterol decreased (P < 0.01). The increase in triglycerides was mitigated with concomitant insulin infusion (P < 0.05 from without insulin). Plasma LCAT activity increased by 17.7 +/- 7.7% after 8 h (P < 0.001) and by 26.1 +/- 11. 1% after 24 h (P < 0.001), PLTP activity increased by 19.7 +/- 15.6% after 24 h (P < 0.001), but CETP activity remained unchanged. Concomitant insulin infusion blunted the increase in plasma LCAT activity (P < 0.05 from without insulin), but not that in PLTP activity. One week after the first fat load, plasma non-HDL cholesterol (P < 0.02), and triglycerides (P = 0.05) were increased, whereas HDL cholesterol was decreased (P < 0.02). Plasma CETP and PLTP activity levels were increased by 34.8 +/- 30.4% (P < 0.02) and by 15.9 +/- 6.4% (P < 0.02), respectively, but LCAT activity was then unaltered. In summary, plasma LCAT, PLTP, and CETP activity levels are stimulated by a large intravenous fat load, but the time course of their responses and the effects of insulin coadministration are different. Changes in plasma LCAT and PLTP activities may be implicated in HDL and triglyceride-rich lipoprotein remodeling under the present experimental conditions.
authors.affiliation: Department of Endocrinology, University Hospital Groningen, 9700 RB Groningen, The Netherlands.
authors.forename: S C
authors.initials: SC
authors.lastname: Riemens
authors.forename: A
authors.initials: A
authors.lastname: Van Tol
authors.forename: W J
authors.initials: WJ
authors.lastname: Sluiter
authors.forename: R P
authors.initials: RP
authors.lastname: Dullaart
mesh_terms: D002352:Carrier Proteins / Q000097:blood*; D053480:Cholesterol Ester Transfer Proteins; D004338:Drug Combinations; D005217:Fat Emulsions, Intravenous / Q000494:pharmacology; D006023:Glycoproteins; D006801:Humans; D007262:Infusions, Intravenous; D007328:Insulin / Q000494:pharmacology; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000097:blood*; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood*; D010713:Phosphatidylcholines / Q000097:blood*; D049294:Phospholipid Transfer Proteins; D010743:Phospholipids / Q000494:pharmacology; D013012:Sorbitol / Q000494:pharmacology; D014280:Triglycerides / Q000494:pharmacology*
chemical_list: C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D004338:Drug Combinations; D005217:Fat Emulsions, Intravenous; D006023:Glycoproteins; D007328:Insulin; D008077:Lipoproteins, LDL; D008565:Membrane Proteins; D010713:Phosphatidylcholines; D049294:Phospholipid Transfer Proteins; D010743:Phospholipids; D014280:Triglycerides; C008288:Lipofundin; D013012:Sorbitol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase