| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Original Studies |
Obstetrical and Gynecological Clinic of the University of Belgrade School of Medicine (N.R., J.D., S.P.), 1000 Belgrade, Yugoslavia; and the Department of Obstetrics and Gynecology, New York University School of Medicine (E.K., T.R., C.J.L.), New York, New York 10016
Address all correspondence and requests for reprints to: Dr. Charles J. Lockwood, Department of Obstetrics and Gynecology, New York University School of Medicine, 550 First Avenue, New York, New York 10016. E-mail: charles.lockwood{at}med.nyu.edu
Apolipoprotein B is elevated in growth-retarded compared with normally grown fetuses, demonstrating a link between low birth weight and risk of subsequent atherosclerosis. Increased apolipoprotein B levels and an elevated apolipoprotein B to A-I ratio are predictors of atherogenesis. Elevated apolipoprotein B levels in young adults have been linked to atherosclerosis in later life, whereas impaired fetal growth has been linked to higher than normal apolipoprotein B levels in adulthood. We conducted this research to test the hypothesis that circulating apolipoprotein A-I and B concentrations differ in growth-retarded compared with normal fetuses. Fetal umbilical plasma samples were obtained at diagnostic cordocenteses in 18 growth-retarded and 23 normally grown fetuses. Levels of apolipoprotein A-I and B were measured by turbidimetric assay. There were no differences in median (range) plasma apolipoprotein A-I concentrations between growth-retarded and normal fetuses [0.61 (0.301.42) vs. 0.60 (0.301.63) g/L, respectively; P = 0.94]. In contrast, we found significantly higher plasma apolipoprotein B levels in growth-retarded vs. normal fetuses [0.62 (0.371.84) vs. 0.40 (0.161.47) g/L, respectively; P < 0.001]. Moreover, the ratio of apolipoprotein B to A-I was significantly higher in growth-retarded than in normal fetuses [1.00 (0.382.42) vs. 0.53 (0.311.80); P = 0.005]. Levels of apolipoprotein B are elevated in growth-retarded fetuses, suggesting a linkage between low birth weight and adult-onset atherosclerosis.
This article has been cited by other articles:
![]() |
Q. Fu, X. Yu, C. W. Callaway, R. H. Lane, and R. A. McKnight Epigenetics: intrauterine growth retardation (IUGR) modifies the histone code along the rat hepatic IGF-1 gene FASEB J, August 1, 2009; 23(8): 2438 - 2449. [Abstract] [Full Text] [PDF] |
||||
![]() |
Z. Wang, Z. Huang, G. Lu, L. Lin, and M. Ferrari Hypoxia during pregnancy in rats leads to early morphological changes of atherosclerosis in adult offspring Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1321 - H1328. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Y. Tomoum, M. M. Awadallah, D. A. Fouad, and A. H. Ali Lipid Profile, Apolipoproteins A and B in Children With Epilepsy J Child Neurol, November 1, 2008; 23(11): 1275 - 1281. [Abstract] [PDF] |
||||
![]() |
C. Wadsack, S. Tabano, A. Maier, U. Hiden, G. Alvino, V. Cozzi, M. Huttinger, W. J. Schneider, U. Lang, I. Cetin, et al. Intrauterine growth restriction is associated with alterations in placental lipoprotein receptors and maternal lipoprotein composition Am J Physiol Endocrinol Metab, February 1, 2007; 292(2): E476 - E484. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. O. Kwiterovich Jr, S. L. Cockrill, D. G. Virgil, E. S. Garrett, J. Otvos, C. Knight-Gibson, P. Alaupovic, T. Forte, L. Zhang, Z. N. Farwig, et al. A Large High-Density Lipoprotein Enriched in Apolipoprotein C-I: A Novel Biochemical Marker in Infants of Lower Birth Weight and Younger Gestational Age JAMA, April 20, 2005; 293(15): 1891 - 1899. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Lauren, M.-R. Jarvelin, P. Elliott, U. Sovio, A. Spellman, M. McCarthy, P. Emmett, I. Rogers, A.-L. Hartikainen, A. Pouta, et al. Relationship between birthweight and blood lipid concentrations in later life: evidence from the existing literature Int. J. Epidemiol., October 1, 2003; 32(5): 862 - 876. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. PALINSKI and C. NAPOLI The fetal origins of atherosclerosis: maternal hypercholesterolemia, and cholesterol-lowering or antioxidant treatment during pregnancy influence in utero programming and postnatal susceptibility to atherogenesis FASEB J, September 1, 2002; 16(11): 1348 - 1360. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. G. IJzerman, C. D. A. Stehouwer, M. M. van Weissenbruch, E. J. de Geus, and D. I. Boomsma Evidence for Genetic Factors Explaining the Association Between Birth Weight and Low-Density Lipoprotein Cholesterol and Possible Intrauterine Factors Influencing the Association Between Birth Weight and High-Density Lipoprotein Cholesterol: Analysis in Twins J. Clin. Endocrinol. Metab., November 1, 2001; 86(11): 5479 - 5484. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Hyka, J.-M. Dayer, C. Modoux, T. Kohno, C. K. Edwards III, P. Roux-Lombard, and D. Burger Apolipoprotein A-I inhibits the production of interleukin-1{beta} and tumor necrosis factor-{alpha} by blocking contact-mediated activation of monocytes by T lymphocytes Blood, April 15, 2001; 97(8): 2381 - 2389. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |