title: Lecithin:cholesterol acyltransferase activity and high-density lipoprotein subfraction composition in type 1 diabetic patients with improving metabolic control.
abstract: On initial diagnosis or when metabolic control is poor, subjects with type 1 (insulin-dependent) diabetes mellitus often exhibit decreased high density lipoprotein (HDL) cholesterol levels, which have been associated in numerous studies in non-diabetic subjects with atherosclerosis and coronary artery disease. We measured the activities of plasma lecithin:cholesterol acyltransferase (LCAT), post-heparin lipoprotein lipase, and the composition of the HDL subfractions HDL2 and HDL3, in ten poorly controlled type 1 diabetic patients admitted to a metabolic ward (six women and four men, aged 18-37 years). The measurements were repeated after metabolic control had been optimised and again a week after discharge. The results were compared with those of ten healthy normolipidaemic subjects matched for age, sex and body mass. LCAT activity increased significantly (P < 0.05) with improved metabolic control in the diabetic patients, and showed positive within-person correlation with HDL2 cholesterol ester (r = 0.67; P < 0.01), HDL2 free cholesterol (r = 0.67; P < 0.01), phosphatidylcholine (r = 0.49; P < 0.05), total phospholipids (r = 0.50; P < 0.01) and apolipoprotein A-I (apo A-I: r = 0.72; P < 0.01). With improving metabolic control HDL2 lipid levels increased more than twofold and the compositional changes in HDL2 were reflected by an increased apo A-I:apo A-II ratio (P < 0.05) and a decreased triglyceride:apo A-I ratio (P < 0.05). Changes in HDL3 levels and composition were minor. The results of this study indicate that an increase in LCAT activity increases the concentration and changes the composition of HDL2 in type 1 diabetic patients with improved metabolic control.
authors.affiliation: National Research Programme for Nutritional Intervention of the Medical Research Council, Tygerberg, Republic of South Africa.
authors.forename: M J
authors.initials: MJ
authors.lastname: Weight
authors.forename: H S
authors.initials: HS
authors.lastname: Coetzee
authors.forename: C M
authors.initials: CM
authors.lastname: Smuts
authors.forename: M P
authors.initials: MP
authors.lastname: Marais
authors.forename: J S
authors.initials: JS
authors.lastname: Maritz
authors.forename: F S
authors.initials: FS
authors.lastname: Hough
authors.forename: A J
authors.initials: AJ
authors.lastname: Benadé
authors.forename: J J
authors.initials: JJ
authors.lastname: Taljaard
mesh_terms: D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood; D002788:Cholesterol Esters / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000201:enzymology; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis*; D006801:Humans; D008071:Lipoprotein Lipase / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D002784:Cholesterol; D002788:Cholesterol Esters; D006442:Glycated Hemoglobin; D008071:Lipoprotein Lipase; D008075:Lipoproteins, HDL; D007862:Phosphatidylcholine-Sterol O-Acyltransferase