title: Is pseudocholinesterase activity related to markers of triacylglycerol synthesis in Type II diabetes mellitus?
abstract: Hypertriglyceridaemia is a risk factor for cardiovascular disease in patients suffering from Type II diabetes mellitus, and is due to enhanced synthesis and/or impaired clearance of triacylglycerol-rich lipoproteins. In the present study we investigated whether pseudocholinesterase (PChE) activity could serve as a marker for the rate of triacylglycerol synthesis in these patients. Patients were stratified according to their apolipoprotein E (apoE) phenotype, i.e. E3E2, E3E3 or E3E4. In study I, the relationship between PChE activity and serum triacylglycerols was investigated in 224 insulin-treated patients with Type II diabetes. In study II, which had a cross-over design, PChE activity was measured in 45 dyslipidaemic, insulin-treated patients with Type II diabetes that were treated with bezafibrate or pravastatin. In study I, PChE activity was correlated positively with serum triacylglycerol concentrations, but did not differ significantly between apoE phenotypes. The strongest relationship was found in the E3E4 group (r=0.50; P=0.001), the phenotype for which hypertriglyceridaemia is expected to be the result of increased triacylglycerol synthesis. In a stepwise multiple regression analysis, serum triacylglycerol concentrations were found to be the strongest predictor of PChE activity in the E3E4 group. In study II, PChE activity decreased as a result of bezafibrate treatment in all three apoE groups. The decrease in PChE activity with bezafibrate treatment paralleled the decrease in serum triacylglycerol concentrations in the apoE subgroups. Pravastatin treatment did not significantly affect PChE activity. Thus the present study suggests an association between PChE activity and the rate of triacylglycerol synthesis. Measurement of PChE activity may therefore be a useful tool in the choice of drug for treatment of hypertriglyceridaemia in patients with Type II diabetes.
authors: Department of Internal Medicine, Ziekenhuis Amstelveen, P.O. Box 328, 1180 AH Amstelveen, The Netherlands. rustemeijer@wxs.nl
authors: C
authors: C
authors: Rustemeijer
authors: J A
authors: JA
authors: Schouten
authors: H J
authors: HJ
authors: Voerman
authors: A C
authors: AC
authors: Beynen
authors: A J
authors: AJ
authors: Donker
authors: R J
authors: RJ
authors: Heine
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001057:Apolipoproteins E; D001629:Bezafibrate / Q000627:therapeutic use*; D015415:Biomarkers; D002091:Butyrylcholinesterase / Q000378:metabolism*; D018592:Cross-Over Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000188:drug therapy / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D016014:Linear Models; D008297:Male; D010641:Phenotype; D017035:Pravastatin / Q000627:therapeutic use; D014280:Triglycerides / Q000096:biosynthesis*
chemical_list: D000924:Anticholesteremic Agents; D001057:Apolipoproteins E; D015415:Biomarkers; D007004:Hypoglycemic Agents; D007328:Insulin; D014280:Triglycerides; D002091:Butyrylcholinesterase; D017035:Pravastatin; D001629:Bezafibrate