LIPOPROTEIN-LIPASE MASS AND ACTIVITY IN SEVERE HYPERTRIGLYCERIDEMIA

被引:114
作者
KOBAYASHI, J
HASHIMOTO, H
FUKAMACHI, I
TASHIRO, J
SHIRAI, K
SAITO, Y
YOSHIDA, S
机构
[1] CHIBA UNIV,SCH MED,DEPT INTERNAL MED 2,1-8-1 INOHANA,CHUOU KU,CHIBA 260,JAPAN
[2] SHIBAYAGI LAB BIOIMMUNOL SCI,CHIBA,JAPAN
[3] TOHO UNIV,DEPT CLIN FUNCT PHYSIOL,FUNABASHI,CHIBA 274,JAPAN
关键词
LIPOPROTEIN LIPASE; IMMUNOASSAY; HUMAN POSTHEPARIN PLASMA LPL; FUNCTIONALLY DEFECTIVE LPL; ELISA;
D O I
10.1016/0009-8981(93)90144-S
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
To clarify the role of defective lipoprotein lipase (LPL) in hypertriglyceridemia, the LPL masses and LPL activities in post-heparin plasma (PHP) were studied in severe hypertriglyceridemias. The developed sandwich enzyme immunoassay for the LPL was sensitive from 0.5 to 20 ng/ml of LPL in human PHP. The plasma LPL mass increased by heparin injection (30 USP units/kg) and was found to positively correlate with LPL activity. The mean LPL activity from PHP of normal controls was 2,960 +/- 1,057 nmol/ml/h. The mean LPL masses from human pre- and 15-min post-heparin plasma from normal subjects were 25 +/- 5 ng/ml and 224 +/- 60 ng/ml, respectively. Thus the specific activity of LPL from PHP of normal controls was calculated to be 13.3 mumol FFA released/h/Ag LPL. Among hypertriglyceridemic patients with over 1,000 mg/dl of serum triglyceride, the incidence of patients with LPL masses less than -2 standard deviations (S.D.) of those of average normal control subjects was found to be 27%. Seventy percent of patients showed specific activities within +2 S.D. of those of average control LPL, and 30% showed significantly low specific activities less than -2 S.D. despite the fact that LPL masses were not less than -2 S.D. of the average normal controls. These results suggest that the evaluation of LPL masses in PHP would be useful for finding functionally defective LPL in patients with hypertriglyceridemia, and that up to 30% severe hypertriglyceridemias may have functionally defective LPL.
引用
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页码:113 / 123
页数:11
相关论文
共 14 条
[1]   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
[2]   DETECTION AND CHARACTERIZATION OF THE HETEROZYGOTE STATE FOR LIPOPROTEIN-LIPASE DEFICIENCY [J].
BABIRAK, SP ;
IVERIUS, PH ;
FUJIMOTO, WY ;
BRUNZELL, JD .
ARTERIOSCLEROSIS, 1989, 9 (03) :326-334
[3]   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
[4]  
BELFRAGE P, 1969, J LIPID RES, V10, P341
[5]  
BRUNZELL JD, 1986, LIPOPROTEIN DEFICIEN, P227
[6]  
CHENG CF, 1985, J BIOL CHEM, V260, P720
[7]  
EMI M, 1990, J BIOL CHEM, V265, P5910
[8]   PRODUCTION AND USE OF AN INHIBITORY MONOCLONAL-ANTIBODY TO HUMAN LIPOPROTEIN-LIPASE [J].
GOLDBERG, IJ ;
PATERNITI, JR ;
FRANCE, DS ;
MARTINELLI, G ;
CORNICELLI, JA .
BIOCHIMICA ET BIOPHYSICA ACTA, 1986, 878 (02) :168-176
[9]   LIPOPROTEIN-LIPASE WITH A DEFECT IN LIPID INTERFACE RECOGNITION IN A CASE WITH TYPE-I HYPERLIPEMIA [J].
KOBAYASHI, J ;
SHIRAI, K ;
SAITO, Y ;
YOSHIDA, S .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 1989, 19 (05) :424-432
[10]  
KOBAYASHI J, 1992, BIOCHEM BIOPH RES CO, V182, P71