Postprandial Increase of Complement Component 3 in Normolipidemic Patients With Coronary Artery Disease
- 1 September 2001
- journal article
- other
- Published by Wolters Kluwer Health in Arteriosclerosis, Thrombosis, and Vascular Biology
- Vol. 21 (9), 1526-1530
- https://doi.org/10.1161/hq0901.095276
Abstract
Plasma concentrations of the third complement component (C3) predict the risk of myocardial infarction. Because chylomicrons stimulate C3 production by adipocytes in vitro, we investigated plasma C3 changes in vivo after an oral fat load. Thirty-seven subjects (20 normolipidemic patients with coronary artery disease [CAD] and 17 healthy control subjects) underwent an oral fat load (50 g/m2). C3 was measured at baseline and at 2-hour intervals after fat intake for 10 hours. The effects of lipid lowering by simvastatin were evaluated in 16 patients. Fasting plasma C3 was 1.06±0.26 and 0.90±0.12 g/L in CAD patients and control subjects, respectively. Fasting C3 was correlated with several parameters associated with insulin resistance. The best determinant of fasting C3 was waist circumference (adjusted R2=0.48, β=0.71, PR2=0.63). Plasma C3 levels at 2, 4, and 6 hours after fat ingestion were significantly higher than fasting levels in patients and control subjects. C3 increased maximally to 1.39±0.33 g/L in patients and to 1.11±0.18 g/L in control subjects (PR2=0.47, β=0.70; PP<0.05 for both versus no treatment). Postprandial plasma C3 concentrations increase in CAD patients and control subjects. Fasting C3 is associated with waist circumference, but postprandial C3 increment is associated with postprandial lipemia. Fasting and postprandial C3 concentrations decrease after treatment with simvastatin.Keywords
This publication has 18 references indexed in Scilit:
- Relationship of serum C3 to fasting insulin, risk factors and previous ischaemic events in middle-aged menEuropean Heart Journal, 2000
- Relationship of serum C3 complement with insulin resistance and coronary heart disease—cause, consequence or common antecedent?Published by Oxford University Press (OUP) ,2000
- The influence of oral lipid loads on acylation stimulating protein (ASP) in healthy volunteersInternational Journal of Obesity, 1998
- Retention of fluorescent‐labelled chylomicron remnants within the intima of the arterial wall — evidence that plaque cholesterol may be derived from post‐prandial lipoproteinsEuropean Journal of Clinical Investigation, 1998
- Serum complement and familial combined hyperlipidemiaAtherosclerosis, 1997
- The adipsin-acylation stimulating protein system and regulation of intracellular triglyceride synthesis.Journal of Clinical Investigation, 1993
- Impaired fatty acid metabolism in familial combined hyperlipidemia. A mechanism associating hepatic apolipoprotein B overproduction and insulin resistance.Journal of Clinical Investigation, 1993
- Modulation of chylomicron remnant metabolism by an hepatic hydroxymethylglutaryl coenzyme A reductase inhibitorMetabolism, 1990
- Evidence for a Common, Saturable, Triglyceride Removal Mechanism for Chylomicrons and Very Low Density Lipoproteins in ManJournal of Clinical Investigation, 1973
- Human C′3: Evidence for the Liver as the Primary Site of SynthesisScience, 1969