Radunovic, Nebojsa (7003538030)Nebojsa (7003538030)RadunovicKuczynski, Edward (7003870928)Edward (7003870928)KuczynskiRosen, Todd (7101634950)Todd (7101634950)RosenDukanac, Jelena (6506093302)Jelena (6506093302)DukanacPetkovic, Spasoje (7005164142)Spasoje (7005164142)PetkovicLockwood, Charles J. (7102516684)Charles J. (7102516684)Lockwood2025-06-132025-06-132000https://doi.org/10.1210/jcem.85.1.6243https://www.scopus.com/inward/record.uri?eid=2-s2.0-0034456308&doi=10.1210%2fjcem.85.1.6243&partnerID=40&md5=5d904a5dd15b8ea90b0c3aa23581b335https://remedy.med.bg.ac.rs/handle/123456789/11253Apolipoprotein 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 (0.30-1.42) vs. 0.60 (0.30-1.63) g/L, respectively; P = 0.94]. In contrast, we found significantly higher plasma apolipoprotein B levels in growthretarded vs. normal fetuses [0.62 (0.37-1.84) vs. 0.40 (0.16-1.47) 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 (0.38-2.42) vs. 0.53 (0.31-1.80); P = 0.005]. Levels of apolipoprotein B are elevated in growth-retarded fetuses, suggesting a linkage between low birth weight and adult-onset atherosclerosis.