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Higher plasma lipid transfer protein activities and unfavorable lipoprotein changes in cigarette-smoking men.
Arterioscler Thromb. 1994 Oct; 14(10):1581-5.AT

Abstract

The mechanism responsible for the atherogenic lipoprotein changes associated with cigarette smoking are largely unknown. Lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) are key factors in the esterification of plasma cholesterol and the transfer of cholesteryl ester from high-density lipoproteins (HDLs) toward very-low- and low-density lipoproteins (VLDLs+LDLs). Another transfer factor, phospholipid transfer protein (PLTP), recently has been shown to be involved in the interconversion of HDL particles in vitro, but its physiological function is not yet clear. We measured the activities of LCAT, CETP (as cholesteryl ester exchange activity), and PLTP using exogenous substrate assays as well as lipoprotein profiles in the plasma of 21 normolipidemic cigarette-smoking men (total plasma cholesterol below 6.5 mmol/L and triglyceride below 2.5 mmol/L) and 21 individually matched nonsmoking control subjects. HDL cholesterol, HDL cholesteryl ester, and plasma apolipoprotein A-I levels were lower in the smokers than in the control subjects (P < or = .05 for all parameters). Median plasma CETP activity was 18% higher (P < .02) and median plasma PLTP activity was 8% higher (P < .05) in the smokers compared with the nonsmokers. LCAT activity was not different between the groups. HDL cholesteryl ester concentration was positively related to LCAT activity in control subjects but not in smokers. By contrast, there was an inverse relation of CETP activity with HDL cholesteryl ester in smokers but not in nonsmokers. Multiple regression analysis demonstrated that the lowering effect of smoking on HDL cholesteryl ester could be explained by its influence on CETP activity.(

ABSTRACT

TRUNCATED AT 250 WORDS)

Authors+Show Affiliations

Department of Endocrinology, State University Hospital Groningen, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

7918308

Citation

Dullaart, R P., et al. "Higher Plasma Lipid Transfer Protein Activities and Unfavorable Lipoprotein Changes in Cigarette-smoking Men." Arteriosclerosis and Thrombosis : a Journal of Vascular Biology, vol. 14, no. 10, 1994, pp. 1581-5.
Dullaart RP, Hoogenberg K, Dikkeschei BD, et al. Higher plasma lipid transfer protein activities and unfavorable lipoprotein changes in cigarette-smoking men. Arterioscler Thromb. 1994;14(10):1581-5.
Dullaart, R. P., Hoogenberg, K., Dikkeschei, B. D., & van Tol, A. (1994). Higher plasma lipid transfer protein activities and unfavorable lipoprotein changes in cigarette-smoking men. Arteriosclerosis and Thrombosis : a Journal of Vascular Biology, 14(10), 1581-5.
Dullaart RP, et al. Higher Plasma Lipid Transfer Protein Activities and Unfavorable Lipoprotein Changes in Cigarette-smoking Men. Arterioscler Thromb. 1994;14(10):1581-5. PubMed PMID: 7918308.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Higher plasma lipid transfer protein activities and unfavorable lipoprotein changes in cigarette-smoking men. AU - Dullaart,R P, AU - Hoogenberg,K, AU - Dikkeschei,B D, AU - van Tol,A, PY - 1994/10/1/pubmed PY - 1994/10/1/medline PY - 1994/10/1/entrez SP - 1581 EP - 5 JF - Arteriosclerosis and thrombosis : a journal of vascular biology JO - Arterioscler. Thromb. VL - 14 IS - 10 N2 - The mechanism responsible for the atherogenic lipoprotein changes associated with cigarette smoking are largely unknown. Lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) are key factors in the esterification of plasma cholesterol and the transfer of cholesteryl ester from high-density lipoproteins (HDLs) toward very-low- and low-density lipoproteins (VLDLs+LDLs). Another transfer factor, phospholipid transfer protein (PLTP), recently has been shown to be involved in the interconversion of HDL particles in vitro, but its physiological function is not yet clear. We measured the activities of LCAT, CETP (as cholesteryl ester exchange activity), and PLTP using exogenous substrate assays as well as lipoprotein profiles in the plasma of 21 normolipidemic cigarette-smoking men (total plasma cholesterol below 6.5 mmol/L and triglyceride below 2.5 mmol/L) and 21 individually matched nonsmoking control subjects. HDL cholesterol, HDL cholesteryl ester, and plasma apolipoprotein A-I levels were lower in the smokers than in the control subjects (P < or = .05 for all parameters). Median plasma CETP activity was 18% higher (P < .02) and median plasma PLTP activity was 8% higher (P < .05) in the smokers compared with the nonsmokers. LCAT activity was not different between the groups. HDL cholesteryl ester concentration was positively related to LCAT activity in control subjects but not in smokers. By contrast, there was an inverse relation of CETP activity with HDL cholesteryl ester in smokers but not in nonsmokers. Multiple regression analysis demonstrated that the lowering effect of smoking on HDL cholesteryl ester could be explained by its influence on CETP activity.(ABSTRACT TRUNCATED AT 250 WORDS) SN - 1049-8834 UR - https://www.unboundmedicine.com/medline/citation/7918308/Higher_plasma_lipid_transfer_protein_activities_and_unfavorable_lipoprotein_changes_in_cigarette_smoking_men_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&amp;PAGE=linkout&amp;SEARCH=7918308.ui DB - PRIME DP - Unbound Medicine ER -