Postprandial lipoprotein metabolism and atherosclerosis

被引：286

作者：

Karpe, F ^{[1
]}

机构：

[1] Radcliffe Infirm, Oxford Lipid Metab Grp, Oxford OX2 6HE, England

[2] Karolinska Hosp, Dept Med, King Gustaf V Res Inst, S-10401 Stockholm, Sweden

来源：

JOURNAL OF INTERNAL MEDICINE | 1999年 / 246卷 / 04期

关键词：

apolipoprotein B-48; apolipoprotein B-100; atherosclerosis; triglyceride-rich lipoproteins; TRL remnants; VLDL;

D O I：

10.1046/j.1365-2796.1999.00548.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Postprandial lipids and lipoproteins have been associated with the presence of cardiovascular disease in a large number of case-control studies. Because the metabolic perturbations around the postprandial situation is a key driving force for cholesterol flux between lipoproteins and tissues, together with the augmented generation of potentially atherogenic cholesterol-rich remnant lipoproteins, several hypotheses have been formulated to link excessive lipoproteinaemic response to fat intake with cardiovascular disease. Recent information on the regulation of lipoprotein remnant formation and its relation Ito atherosclerosis will enable us to test a pertinent clinical question: is there a direct relationship between repeated elevations of postprandial lipoproteins and development of atherosclerosis?

引用

页码：341 / 355

页数：15

共 120 条

[1] MECHANISM OF HYPERTRIGLYCERIDEMIA IN HUMAN APOLIPOPROTEIN-(APO)-CIII TRANSGENIC MICE - DIMINISHED VERY LOW-DENSITY-LIPOPROTEIN FRACTIONAL CATABOLIC RATE ASSOCIATED WITH INCREASED APO-CIII AND REDUCED APO-E ON THE PARTICLES
AALTOSETALA, K
FISHER, EA
CHEN, XL
CHAJEKSHAUL, T
HAYEK, T
ZECHNER, R
WALSH, A
RAMAKRISHNAN, R
GINSBERG, HN
BRESLOW, JL
[J]. JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (05) : 1889 - 1900
[2] INTERACTION OF LPB, LPB-E, LPB-C-III, AND LPB-C-III-E LIPOPROTEINS WITH THE LOW-DENSITY-LIPOPROTEIN RECEPTOR OF HELA-CELLS
AGNANI, G
BARD, JM
CANDELIER, L
DELATTRE, S
FRUCHART, JC
CLAVEY, V
[J]. ARTERIOSCLEROSIS AND THROMBOSIS, 1991, 11 (04): : 1021 - 1029
[3] The role of triglyceride-rich lipoprotein families in the progression of atherosclerotic lesions as determined by sequential coronary angiography from a controlled clinical trial
Alaupovic, P
Mack, WJ
KnightGibson, C
Hodis, HN
[J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (04) : 715 - 722
[4] Prolonged postprandial responses of lipids and apolipoproteins in triglyceride-rich lipoproteins of individuals expressing an apolipoprotein epsilon 4 allele
Bergeron, N
Havel, RJ
[J]. JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (01) : 65 - 72
[5] Björkegren J, 1998, J LIPID RES, V39, P1412
[6] Bjorkegren J, 1996, J LIPID RES, V37, P76
[7] Bjorkegren J, 1997, J LIPID RES, V38, P301
[8] Identification of the principal proteoglycan-binding site in LDL -: A single-point mutation in apo-B100 severely affects proteoglycan interaction without affecting LDL receptor binding
Borén, J
Olin, K
Lee, I
Chait, A
Wight, TN
Innerarity, TL
[J]. JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (12) : 2658 - 2664
[9] CHYLOMICRON-REMNANT CLEARANCE IN HOMOZYGOTE AND HETEROZYGOTE WATANABE-HERITABLE-HYPERLIPEMIC RABBITS IS DEFECTIVE - LACK OF EVIDENCE FOR AN INDEPENDENT CHYLOMICRON-REMNANT RECEPTOR
BOWLER, A
REDGRAVE, TG
MAMO, JCL
[J]. BIOCHEMICAL JOURNAL, 1991, 276 : 381 - 386
[10] EVIDENCE FOR A COMMON, SATURABLE, TRIGLYCERIDE REMOVAL MECHANISM FOR CHYLOMICRONS AND VERY LOW-DENSITY LIPOPROTEINS IN MAN
BRUNZELL, JD
HAZZARD, WR
PORTE, D
BIERMAN, EL
[J]. JOURNAL OF CLINICAL INVESTIGATION, 1973, 52 (07) : 1578 - 1585

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