Lipoprotein lipase: Physiology, biochemistry, and molecular biology

被引：146

作者：

Goldberg, IJ

Merkel, M

机构：

[1] Columbia Univ Coll Phys & Surg, Div Prevent Med & Nutr, New York, NY 10032 USA

[2] Univ Hamburg, Hosp Eppendorf, Dept Internal Med, D-20246 Hamburg, Germany

来源：

FRONTIERS IN BIOSCIENCE-LANDMARK | 2001年 / 6卷

关键词：

triglyceride; chylomicrons; heparin; proteoglycans; hyperlpidemai; review;

D O I：

10.2741/Goldberg

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：

Lipoprotein lipase (LpL) is the primary enzyme responsible for conversion of lipoprotein triglyceride into free fatty acids and monoglyderides. This permits their uptake into muscle and adipose. The roles of this enzyme in normal and altered physiology are reviewed. In addition, the relationship of LpL activity and genetic variations of LpL and human disease are summarized.Lipoprotein lipase (LpL) is the primary enzyme responsible for conversion of lipoprotein triglyceride into free fatty acids and monoglyderides. This permits their uptake into muscle and adipose. The roles of this enzyme in normal and altered physiology are reviewed. In addition, the relationship of LpL activity and genetic variations of LpL and human disease are summarized.

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页码：D388 / D405

页数：18

相关论文

共 201 条

[1] INTESTINAL EXPRESSION OF HUMAN APOLIPOPROTEIN A-IV IN TRANSGENIC MICE FAILS TO INFLUENCE DIETARY-LIPID ABSORPTION OR FEEDING-BEHAVIOR [J].

AALTOSETALA, K ;

BISGAIER, CL ;

HO, A ;

KIEFT, KA ;

TRABER, MG ;

KAYDEN, HJ ;

RAMAKRISHNAN, R ;

WALSH, A ;

ESSENBURG, AD ;

BRESLOW, JL .

JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (04) :1776-1786

[2] 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 [J].

AALTOSETALA, K ;

FISHER, EA ;

CHEN, XL ;

CHAJEKSHAUL, T ;

HAYEK, T ;

ZECHNER, R ;

WALSH, A ;

RAMAKRISHNAN, R ;

GINSBERG, HN ;

BRESLOW, JL .

JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (05) :1889-1900

[3] FAMILIAL CHYLOMICRONEMIA (TYPE-I HYPERLIPOPROTEINEMIA) DUE TO A SINGLE MISSENSE MUTATION IN THE LIPOPROTEIN-LIPASE GENE [J].

AMEIS, D ;

KOBAYASHI, J ;

DAVIS, RC ;

BENZEEV, O ;

MALLOY, MJ ;

KANE, JP ;

LEE, G ;

WONG, H ;

HAVEL, RJ ;

SCHOTZ, MC .

JOURNAL OF CLINICAL INVESTIGATION, 1991, 87 (04) :1165-1170

[4] THE VERY-LOW-DENSITY LIPOPROTEIN RECEPTOR MEDIATES THE CELLULAR CATABOLISM OF LIPOPROTEIN-LIPASE AND UROKINASE-PLASMINOGEN ACTIVATOR INHIBITOR TYPE-I COMPLEXES [J].

ARGRAVES, KM ;

BATTEY, FD ;

MACCALMAN, CD ;

MCCRAE, KR ;

GAFVELS, M ;

KOZARSKY, KF ;

CHAPPELL, DA ;

STRAUSS, JF ;

STRICKLAND, DK .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (44) :26550-26557

[5]

Baum L, 1999, AM J MED GENET, V88, P136, DOI 10.1002/(SICI)1096-8628(19990416)88:2<136::AID-AJMG8>3.0.CO

[6]

2-D

[7] LIPOPROTEIN-LIPASE BETHESDA - A SINGLE AMINO-ACID SUBSTITUTION (ALA-176-]THR) LEADS TO ABNORMAL HEPARIN BINDING AND LOSS OF ENZYMATIC-ACTIVITY [J].

BEG, OU ;

MENG, MS ;

SKARLATOS, SI ;

PREVIATO, L ;

BRUNZELL, JD ;

BREWER, HB ;

FOJO, SS .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (09) :3474-3478

[8] LIPOPROTEIN-LIPASE ENHANCES THE BINDING OF CHYLOMICRONS TO LOW-DENSITY-LIPOPROTEIN RECEPTOR-RELATED PROTEIN [J].

BEISIEGEL, U ;

WEBER, W ;

BENGTSSONOLIVECRONA, G .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (19) :8342-8346

[9]

Benlian P, 1996, AM J HUM GENET, V59, P431

[10] Premature atherosclerosis in patients with familial chylomicronemia caused by mutations in the lipoprotein lipase gene [J].

Benlian, P ;

DeGennes, JL ;

Foubert, L ;

Zhang, HF ;

Gagne, SE ;

Hayden, M .

NEW ENGLAND JOURNAL OF MEDICINE, 1996, 335 (12) :848-854

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