冠動脈症患における動脈硬化性レムナントとしての中間比重リポ蛋白(IDL)とアポ蛋白B48の関与について

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タイトル別名
  • Intermediate-density lipoprotein as an indipendent risk factor for coronary artery disease

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A large number of basic and clinical studies have demonstrated that triglyceride-rich lipoproteins (TRLP) are atherogenenic. Some have also demonstrated that the metabolism of exogenous lipoproteins containing apolipoprotein (apo) B48 in postprandial lipemia is related to the development of atherosclerosis. The purpose of this study is to investigate whether triglyceride (TG)-rich remnant lipoproteins are related to atherosclerotic coronary artery disease (CAD) and whether this relationship is affected by metabolic states in which apo B48 remains in fasting plasma. We evaluated the levels of lipids, apoproteins, and cholesterol (C) levels of VLDL, IDL, and LDL fractions that were separated by ultracentrifugation (VLDL-C, IDL-C, LDL-C) in fasting plasma from 209 consecutive patients who underwent coronary angiography. We also examined apo B48 in VLDL fractions by SDS-PAGE to detect the presence of chylomicron remnants. Patients taking lipid-lowering Burgs were excluded. Patients with CAD (+), defined as≥50% stenosis in the major coronary artery (n=159, mean age 60), were older than CAD (-) (n=50, mean age 55). CAD (+) had significantly higher levels of apo B and lower levels of HDL-C and apo AT compared to CAD (-). The total-C, TG and lipoprotein (a) levels were not significantly different. Although the VLDL-C levels were not significantly different, the levels of IDL-C and LDL-C were significantly higher in CAD (+) than in CAD (-). The presence of apo B48 tended to be more frequent in CAD patients and was significantly related to elevated levels of total-C, TG, VLDL-C, and reduced levels of HDL-C, respectively. In multiple logistic regression analysis, IDL-C and HDL-C were significantly and independently associated with CAD. In conclusion, elenated IDI-C of TRLP and reduced HDL-C are independent predictors of CAD. Furthermore, metabolic disorder of apo B48 containing exogenous lipoproteins may contribute to increasing atherogenic of endogenous lipoproteins.

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