Effects of atorvastatin on fasting and postprandial complement component 3 response in familial combined hyperlipidemia

Caroline Verseyden, Sharon Meijssen, Hans van Dijk, Hans Jansen, and Manuel Castro Cabezas

Internal Medicine, University Medical Center Utrecht, Utrecht 3584 CX

Corresponding Author: m.castrocabezas{at}azu.nl

VLDL overproduction by enhanced hepatic FFA flux, is a major characteristic in familial combined hyperlipidemia (FCHL). The postprandial complement component 3 (C3) response has been associated to impaired postprandial FFA metabolism in FCHL. We investigated the effects of 16 weeks treatment with atorvastatin on postprandial C3 and lipid changes in 12 FCHL patients. Atorvastatin significantly lowered fasting plasma C3 and TG in FCHL. Fasting TG and insulin sensitivity were the best predictors of fasting and postprandial C3. Postprandial triglyceridemia and C3 response, estimated as area under the curve (AUC), were significantly lowered by atorvastatin by 19% and 12%, respectively, albeit still elevated compared to 10 matched controls. Postprandial FFA-AUC and post-heparin plasma lipolytic activities remained unchanged after atorvastatin, suggesting no major effect on lipolysis. After atorvastatin, postprandial hydroxybutyric acid (HBA)-AUC, which was elevated in untreated FCHL, decreased by atorvastatin reaching similar values as in controls. The present data show reduction of postprandial hepatic FFA flux in FCHL by atorvastatin, providing an additional mechanistic explanation for the reduction of VLDL secretion reported earlier for atorvastatin. This was accompanied by a decrease of fasting plasma C3 concentrations and a blunted postprandial C3 response to an acute oral fat load.

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				C. Verseyden, S. Meijssen, and M. C. Cabezas Effects of Atorvastatin on Fasting Plasma and Marginated Apolipoproteins B48 and B100 in Large, Triglyceride-Rich Lipoproteins in Familial Combined Hyperlipidemia J. Clin. Endocrinol. Metab., October 1, 2004; 89(10): 5021 - 5029. [Abstract] [Full Text] [PDF]