The metabolic syndrome in relation to complement component 3 and postprandial lipemia in patients from an outpatient lipid clinic and healthy volunteers

• Published in: Atherosclerosis Vol. 190; no. 1; pp. 167 - 173
• Main Authors: van Oostrom, Antonie J.H.H.M., Alipour, Arash, Plokker, Thijs W.M., Sniderman, Alan D., Cabezas, Manuel Castro
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Ireland Ltd 01.01.2007; Elsevier
• Subjects: Adult; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Biomarkers - blood; Blood and lymphatic vessels; Cardiology. Vascular system; Cardiovascular; Complement C3 - metabolism; Complement component 3; Diabetes Mellitus, Type 2 - immunology; Diabetes Mellitus, Type 2 - metabolism; Fatty acids; Fatty Acids - blood; Female; General and cellular metabolism. Vitamins; Homeostasis - physiology; Humans; Hyperlipidemias - immunology; Hyperlipidemias - metabolism; Insulin Resistance; Lipids; Male; Medical sciences; Metabolic syndrome; Metabolic Syndrome - immunology; Metabolic Syndrome - metabolism; Middle Aged; Outpatients; Pharmacology. Drug treatments; Postprandial; Postprandial Period; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Triglycerides - blood; Lipids; Complement component 3; Metabolic syndrome; Postprandial; Fatty acids; Endocrinopathy; Human; Pancreatic hormone; Fasting; Complement C3; Oral administration; Metabolic diseases; Cardiovascular disease; Free fatty acid; Triglyceride; Insulin; Vascular disease; Lipemia; X Syndrome; Atherosclerosis; Ambulatory; Comparative study
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/j.atherosclerosis.2006.01.009

We investigated the relationship between complement component 3 (C3), fasting and postprandial lipemia and the metabolic syndrome (MetabS). Herefore fasting and postprandial samples after an acute oral fat load were obtained in 40 MetabS+ (50 ± 8 years) and 70 MetabS− (48 ± 7 years) subjects. Fasting C3 was higher in MetabS+ (1.21 ± 0.33 g/L versus 0.91 ± 0.14 g/L, P < 0.001). Postprandially, MetabS+ had a higher total and incremental triglyceride response (TG-AUC: +77%; P < 0.001 and TG-dAUC: +48%; P < 0.05, respectively) and a higher total free fatty acid (FFA-AUC: +13%, P < 0.05) and C3 response (C3-AUC: +26%, P < 0.001) when compared to MetabS−. In both groups, fasting C3 was strongly associated with fasting TG, TG-AUC, TG-dAUC and insulin sensitivity (HOMA) ( R = 0.68, 0.67, 0.41 and 0.67, respectively, for the whole group; P < 0.001 for each). Fasting C3 showed a dose-dependent relation with the number of MetabS components and, following exclusion of these components, it was after TG-AUC, the second best determinant of the MetabS (adjusted R 2 = 0.47, P < 0.001). In conclusion, C3 and postprandial lipema are closely associated with the metabolic syndrome and with several metabolic variables linked to insulin resistance. C3 may be a useful marker to identify subjects with the metabolic syndrome.