Hypertriglyceridemic hyperapoB: The unappreciated atherogenic dyslipoproteinemia in type 2 diabetes mellitus

被引:222
作者
Sniderman, AD
Scantlebury, T
Cianflone, K
机构
[1] McGill Univ, Ctr Hlth, Montreal, PQ, Canada
[2] Concordia Univ, Montreal, PQ, Canada
关键词
D O I
10.7326/0003-4819-135-6-200109180-00014
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Abnormalities in insulin and glucose metabolism do not seem to entirely account for the high frequency of cardiovascular disease in patients with type 2 diabetes mellitus. An important additional factor may be hypertriglyceridemic hyperapoB, an atherogenic dysilpoproteinemia that is common in these patients. The major features of hypertriglyceridemic hyperapoB are hypertriglyceridemia; low levels of high-density lipoprotein cholesterol; and increased numbers of small, dense low-density lipoprotein (LDL) particles. This article reviews the pathophysiology of this disorder, focusing on the changes in lipoprotein particle number and composition rather than lipoprotein lipid levels. The in vitro and in vivo evidence that small, dense LDL are more atherogenic than normal larger, buoyant LDL is summarized, and the particularly high-risk state conferred by increased numbers of small, dense LDL is delineated. This review demonstrates how abnormalities in the plasma lipoproteins may relate to the effectiveness with which adipose tissue traps and retains fatty acid. The effects of increased fatty acid flux on the hepatic metabolism of lipids and apoB secretion are detailed, and the mechanisms by which fibrates and statins may improve these are described. An understanding of these principles should provide the physician with a more physiologic basis on which to choose appropriate therapy.
引用
收藏
页码:447 / 459
页数:13
相关论文
共 146 条
[1]   Metabolic modes of action of the statins in the hyperlipoproteinemias [J].
Aguilar-Salinas, CA ;
Barrett, H ;
Schonfeld, G .
ATHEROSCLEROSIS, 1998, 141 (02) :203-207
[2]   The effect of aggressive and moderate lowering of LDL-cholesterol and low dose anticoagulation on plasma lipids, apolipoproteins and lipoprotein families in post coronary artery bypass graft trial [J].
Alaupovic, P ;
Fesmire, JD ;
Hunnighake, D ;
Domanski, M ;
Forman, S ;
Knatterud, GL ;
Forrester, J ;
Herd, JA ;
Hoogwerf, B ;
Campeau, L ;
Gobel, FL .
ATHEROSCLEROSIS, 1999, 146 (02) :369-379
[3]  
ALBERS JJ, 1992, CLIN CHEM, V38, P658
[4]   Influence of plasma lipid and LDL-subfraction profile on the interaction between low density lipoprotein with human arterial wall proteoglycans [J].
Anber, V ;
Griffin, BA ;
McConnell, M ;
Packard, CJ ;
Shepherd, J .
ATHEROSCLEROSIS, 1996, 124 (02) :261-271
[5]  
Austin MA, 1999, AM J CARDIOL, V83, p13F
[6]  
AUSTIN MA, 1988, JAMA-J AM MED ASSOC, V260, P1917
[7]  
BARBIR M, 1988, BRIT HEART J, V60, P397
[8]   Accumulation of lipoprotein fractions and subfractions in the arterial wall, determined in an in vitro perfusion system [J].
Bjornheden, T ;
Babyi, A ;
Bondjers, G ;
Wiklund, O .
ATHEROSCLEROSIS, 1996, 123 (1-2) :43-56
[9]   GLYCOSYLATED LOW-DENSITY-LIPOPROTEIN IS MORE SENSITIVE TO OXIDATION - IMPLICATIONS FOR THE DIABETIC PATIENT [J].
BOWIE, A ;
OWENS, D ;
COLLINS, P ;
JOHNSON, A ;
TOMKIN, GH .
ATHEROSCLEROSIS, 1993, 102 (01) :63-67
[10]  
Bredie SJH, 1997, ARTERIOSCL THROM VAS, V17, P1465