Maternal and fetal modulators of lipid metabolism correlate with the development of preeclampsia

被引:60
作者
Murai, JT
Muzykanskiy, E
Taylor, RN
机构
[1] UNIV CALIF SAN FRANCISCO,DEPT OBSTET GYNECOL & REPROD SCI,CTR REPROD ENDOCRINOL,SAN FRANCISCO,CA 94143
[2] GERON,MENLO PK,CA
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 1997年 / 46卷 / 08期
关键词
D O I
10.1016/S0026-0495(97)90088-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The pregnancy syndrome preeclampsia is associated with placental dysfunction, dyslipidemia, and endothelial cell activation, and is a major cause of maternal and fetal morbidity and mortality. In this report, a nested case-control study of matched preeclamptic and normal pregnant women was used to investigate the association of maternal and fetal modulators of lipid metabolism with pregnancy outcome. Maternal body mass index (BMI), triglyceride levels, and nonesterified fatty acid (NEFA) concentrations were all significantly increased in women who developed preeclampsia (P < .01). Human placental lactogen (hPL), which is secreted by the syncytiotrophoblast layer of the fetal placenta and reportedly has lipolytic activity, also was found to be elevated in women with preeclampsia (P < .01). By contrast, hemoglobin levels were not found to be statistically different between the two groups of women, indicating that the increased plasma lipids and hPL were not a result of hemoconcentration in preeclamptic patients. The results suggest a multihit hypothesis for the pathophysiology of preeclampsia in which maternal obesity and a placental lipolytic hormone (hPL) converge to adversely affect free fatty acid concentrations in the maternal circulation. Copyright (C) 1997 by W.B. Saunders Company.
引用
收藏
页码:963 / 967
页数:5
相关论文
共 34 条
[1]  
American College of Obstetricians and Gynecologists, 1996, ACOG TECH B, V219, P1
[2]   Plasma factors that determine endothelial cell lipid toxicity in vitro correctly identify women with preeclampsia in early and late pregnancy [J].
Arbogast, BW ;
Leeper, SC ;
Merrick, RD ;
Olive, KE ;
Taylor, RN .
HYPERTENSION IN PREGNANCY, 1996, 15 (03) :263-279
[3]  
BOWER S, 1993, OBSTET GYNECOL, V82, P78
[4]   DIET AND BODY-COMPOSITION AS DETERMINANTS OF BASAL LIPOLYSIS IN HUMANS [J].
CALLESESCANDON, J ;
DRISCOLL, P .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1995, 61 (03) :543-548
[5]   TROPHOBLAST DEPORTATION IN PREECLAMPTIC PREGNANCY [J].
CHUA, S ;
WILKINS, T ;
SARGENT, I ;
REDMAN, C .
BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY, 1991, 98 (10) :973-979
[6]   GENETICS OF PREECLAMPSIA [J].
COOPER, DW ;
BRENNECKE, SP ;
WILTON, AN .
HYPERTENSION IN PREGNANCY, 1993, 12 (01) :1-23
[7]   Biochemical evidence of impaired trophoblastic invasion of decidual stroma in women destined to have preeclampsia [J].
deGroot, CJM ;
OBrien, TJ ;
Taylor, RN .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1996, 175 (01) :24-29
[8]   PLASMA FROM PREECLAMPTIC WOMEN INCREASES HUMAN ENDOTHELIAL-CELL PROSTACYCLIN PRODUCTION WITHOUT CHANGES IN CELLULAR ENZYME-ACTIVITY OR MASS [J].
DEGROOT, CJM ;
DAVIDGE, ST ;
FRIEDMAN, SA ;
MCLAUGHLIN, MK ;
ROBERTS, JM ;
TAYLOR, RN .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1995, 172 (03) :976-985
[9]   INCREASED LIPOLYTIC-ACTIVITY AND HIGH RATIO OF FREE FATTY-ACIDS TO ALBUMIN IN SERA FROM WOMEN WITH PREECLAMPSIA LEADS TO TRIGLYCERIDE ACCUMULATION IN CULTURED ENDOTHELIAL-CELLS [J].
ENDRESEN, MJ ;
LORENTZEN, B ;
HENRIKSEN, T .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1992, 167 (02) :440-447
[10]  
GIFFORD RW, 1991, NIH PUBLICATION, P1