Novel genes for familial combined hyperlipidemia

被引：45

作者：

Aouizerat, BE

Allayee, H

Bodnar, J

Krass, KL

Peltonen, L

de Bruin, TWA

Rotter, JI

Lusis, AJ

机构：

[1] Univ Calif Los Angeles, Dept Med, Div Cardiol, Los Angeles, CA 90095 USA

[2] Univ Calif Los Angeles, Dept Microbiol & Mol Genet, Los Angeles, CA 90024 USA

[3] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90024 USA

[4] Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90024 USA

[5] Natl Publ Hlth Inst, Dept Human Genet, Helsinki, Finland

[6] Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Med & Endocrionl, Maastricht, Netherlands

[7] Steven Spielberg Pediat Res Ctr, Dept Med, Div Med Genet, Los Angeles, CA USA

[8] Steven Spielberg Pediat Res Ctr, Dept Pediat, Los Angeles, CA USA

来源：

CURRENT OPINION IN LIPIDOLOGY | 1999年 / 10卷 / 02期

关键词：

D O I：

10.1097/00041433-199904000-00005

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Familial combined hyperlipidemia (FCHL) is a complex genetic disorder of unknown etiology. Recently, 'modifier' genes of the FCHL phenotype, such as the apolipoprotein AI-CIII-AIV gene cluster and LPL, have been identified in several populations. A 'major' gene for FCHL has been identified in a Finnish isolate which maps to a region syntenic to murine chromosome 3 where a locus for combined hyperlipidemia has been identified. We review these and other recent studies which indicate that FCHL is genetically heterogeneous. Curr Opin Lipidol 10:113-122. (C) 1999 Lippincott Williams & Wilkins.

引用

页码：113 / 122

页数：10

共 77 条

[1] Defects of insulin action on fatty acid and carbohydrate metabolism in familial combined hyperlipidemia [J].