Corticotropin-induced reduction of plasma lipoprotein(a) concentrations in healthy individuals and hemodialysis patients: Relation to apolipoprotein(a) size polymorphism

被引:11
作者
Arnadottir, M [1 ]
Berg, AL
Kronenberg, F
Lingenhel, A
Hugosson, T
Hegbrant, J
Nilsson-Ehle, P
机构
[1] Natl Univ Hosp Reykjavik, Dept Med, IS-101 Reykjavik, Iceland
[2] Univ Lund Hosp, Dept Nephrol, S-22185 Lund, Sweden
[3] Univ Lund Hosp, Dept Clin Chem, S-22185 Lund, Sweden
[4] Univ Innsbruck, Inst Med Biol & Human Genet, A-6020 Innsbruck, Austria
[5] Gambro Grp Renal Care, Lund, Sweden
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 1999年 / 48卷 / 03期
关键词
D O I
10.1016/S0026-0495(99)90083-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Lipoprotein(a) [Lp(a)] a strong independent cardiovascular risk factor, consists of the unique apolipoprotein(a) [apo(a)] covalently linked to a low-density lipoprotein particle. Apo(a) contains a widely differing number of the plasminogen-like kringle IV, a size polymorphism that is codominantly inherited. In addition to powerful genetic control, renal failure is known to influence the plasma Lp(a) concentration. There is still a lot to be learned about the mode and site of catabolism of Lp(a), and there is no readily applicable Lp(a)-lowering treatment available. Therefore, it was of Interest to study further the Lp(a)-lowering effect of corticotropin (ACTH) that has been demonstrated in small studies. The main purpose of the present study was to investigate the influence of ACTH on different apo(a) isoforms, Short-term treatment with ACTH decreased the plasma Lp(a) concentration in all 26 study participants. The two study groups (12 healthy individuals and 14 hemodialysis patients) responded similarly, with a median decrease in plasma Lp(a) of 39% and 49%, respectively in subjects with two clearly separable apo( a) bands, apo(a) phenotyping and densitometric scanning of the bands before and after treatment with ACTH revealed a change in the proportion of apo(a) isoforms, ie, a shift toward the isoform with lower molecular weight. This was observed in seven of nine investigated subjects (four of five healthy individuals and three of four hemodialysis patients). Copyright (C) 1999 by W.B. Saunders Company.
引用
收藏
页码:342 / 346
页数:5
相关论文
共 27 条
[1]   Adrenocorticotrophic hormone lowers serum Lp(a) and LDL cholesterol concentrations in hemodialysis patients [J].
Arnadottir, M ;
Berg, AL ;
Dallongeville, J ;
Fruchart, JC ;
NilssonEhle, P .
KIDNEY INTERNATIONAL, 1997, 52 (06) :1651-1655
[2]   Serum lipoprotein (a) concentration is increased in moderate renal failure [J].
Arnadottir, M ;
Thysell, H ;
NilssonEhle, P .
NEPHRON, 1996, 72 (04) :712-713
[3]   Corticotropin increases the receptor-specific uptake of native low-density lipoprotein (LDL) - But not of oxidized LDL and native or oxidized lipoprotein(a) [Lp(a)] - In HEPG2 cells: No evidence for Lp(a) catabolism via the LDL-receptor [J].
Bartens, W ;
KramerGuth, A ;
Wanner, C .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1997, 46 (07) :726-729
[4]   ACTH lowers serum lipids in steroid-treated hyperlipemic patients with kidney disease [J].
Berg, AL ;
NilssonEhle, P .
KIDNEY INTERNATIONAL, 1996, 50 (02) :538-542
[5]   DIRECT EFFECTS OF CORTICOTROPIN ON PLASMA-LIPOPROTEIN METABOLISM IN MAN - STUDIES IN-VIVO AND IN-VITRO [J].
BERG, AL ;
NILSSONEHLE, P .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1994, 43 (01) :90-97
[6]   Regulation of hepatic lipase secretion from Hep G2 cells by ACTH and corticosteroids [J].
Berg, AL ;
NilssonEhle, P .
HORMONE AND METABOLIC RESEARCH, 1997, 29 (09) :475-476
[7]   APOLIPOPROTEIN(A) GENE ACCOUNTS FOR GREATER THAN 90-PERCENT OF THE VARIATION IN PLASMA LIPOPROTEIN(A) CONCENTRATIONS [J].
BOERWINKLE, E ;
LEFFERT, CC ;
LIN, JP ;
LACKNER, C ;
CHIESA, G ;
HOBBS, HH .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (01) :52-60
[8]   LIPOPROTEIN LP(A) LEVELS ARE REDUCED BY DANAZOL, AN ANABOLIC-STEROID [J].
CROOK, D ;
SIDHU, M ;
SEED, M ;
ODONNELL, M ;
STEVENSON, JC .
ATHEROSCLEROSIS, 1992, 92 (01) :41-47
[9]   ELEVATED PLASMA-CONCENTRATIONS OF LIPOPROTEIN(A) IN PATIENTS WITH END-STAGE RENAL-DISEASE ARE NOT RELATED TO THE SIZE POLYMORPHISM OF APOLIPOPROTEIN(A) [J].
DIEPLINGER, H ;
LACKNER, C ;
KRONENBERG, F ;
SANDHOLZER, C ;
LHOTTA, K ;
HOPPICHLER, F ;
GRAF, H ;
KONIG, P .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 91 (02) :397-401
[10]  
KRAFT HG, 1992, HUM GENET, V90, P220