Low somatomedin activity in cord serum from infants with intrauterine growth retardation

Foley, Thomas P.; DePhilip, Robert M.; Perricelli, Anita; Miller, Arthur S.

doi:10.1016/s0022-3476(80)80874-2

Cited by 56 publications

(29 citation statements)

References 25 publications

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“…Since in the fetal cartilage assay-parallel dose responses were always obtained between test plasma from growth-retarded fetuses and the standard rat plasma, there was no evidence for the presence of inhibitory factors to cartilage sulfation. The present results support those of Foley et al (24) who found somatomedin levels in the cord blood of the human growth-retarded infant to be lower than those of normally grown infants.…”

Section: Discussionsupporting

confidence: 93%

Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

et al. 1984

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ABSTRACT. In this study, the experimental model of Wigglesworth was used to limit the maternal blood supply to the rat fetus and induce intrauterine growth retardation. The associated changes in plasma somatomedin activity, insulin, glucose, and cartilage metabolic activity are reported. The mean body weight (f SEM) of 108 fetuses in ligated uterine horns was significantly lower than that of 146 control fetuses (ligated, 2820 f 50 mg; control, 3180 MSA, multiplication-stimulating activityThe growth hormone-dependent peptide growth factors, the somatomedins, have a major role in the growth and development of skeletal and somatic tissues in postnatal life (1). Somatomedins also are present in the fetus and a positive correlation between circulating levels and fetal body size led us and others to hypothesize that somatomedins providean important anabolic stimulus to development in utero (2-5). However, the factors controlling circulating levels of somatomedins in the fetus are not understood. Growth hormone does not appear to be important since decapitation of the fetal rabbit and hypophysectomy of the lamb in utero did not lower somatomedin bio-and radioreceptor

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Section: Discussionsupporting

confidence: 93%

Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

et al. 1984

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“…In the 16 subjects with IUGR, IGF-I levels were significantly lower than in normal fetuses of the same age, whereas IGF-I1 levels were similar. Our earlier findings that 19-to 24-wk-old hypotrophic fetuses have depressed serum growth-promoting activity (37) are relevant here, as is an earlier report showing low somatomedin activity in cord serum from infants with IUGR (38). DeChiara et al (39) have recently used homologous recombination to obtain heterozygous mice that cany an inactivated IGF-I1 gene and that as a result are growth deficient.…”

Section: Bp (Or Igf-bp) Igf Binding Proteinmentioning

confidence: 61%

Serum Insulin-Like Growth Factors and Insulin-Like Growth Factor Binding Proteins in the Human Fetus. Relationships with Growth in Normal Subjects and in Subjects with Intrauterine Growth Retardation

et al. 1991

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ABSTRACT'. IGF-I, IGF-11, and their binding proteins (BP) were studied in sera obtained by direct puncture of umbilical cords in utero between 20 and 37 wk of gestation in 103 normal fetuses and in 16 fetuses with intrauterine growth retardation, as well as in the cord blood of 37 normal newborns of 38-to 42-wk pregnancies. In normal fetuses, IGF-I levels were approximately 50 ng/mL and IGF-I1 levels approximately 350 ng/mL up to the 33rd wk of pregnancy. Thereafter, both increased to reach values two to three times higher at term. Correlations were found between fetal placental lactogen levels and those of IGF-I and IGF-11, which is consistent with the hypothesis that placental lactogen is involved in the regulation of IGF synthesis in the fetus. With weight (either measured at birth or deduced from echographical data) as index of fetal size, IGF-I levels were significantly ( p < 0.001) higher in fetuses with weights above the mean for gestational age than in fetuses with weights below the mean, whereas IGF-I1 levels were similar in the two groups. Similarly, IGF-I (but not IGF-11) levels in fetuses with intrauterine growth retardation were significantly lower than those in normal fetuses of the same age ( p < 0.01). These findings suggest that, during the latter months of intrauterine life, IGF-I (but not IGF-11) is involved in the control of fetal size. Total fetal BP concentrations were approximately '/J those of adults. The fetal electrophoretic profile obtained by Western-ligand blotting bore a strong resemblance to that of subjects with growth hormone deficiency. In newborns, the proportions of IGF-I and IGF-I1 associated with BP to form 150-kD complexes were considerably lower than those in adults, but similar to those in hypopituitary patients. It may be deduced from these findings that during fetal life, BP synthesis is adapted to increase the bioavailability of the IGF at a time when growth is at a maximum.

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“…In the human newborn, somatomedin levels are low when measured as sulfation bioactivity (20)(21)(22)(23), radioreceptor activity (1,24), and radioimmunoassay (3,(25)(26)(27)(28). Moreover, preterm newborns have lower cord blood somatomedin values than fullterm newborns (1, 2 1, 23, 29).…”

Section: Discussionmentioning

confidence: 99%

Serum Somatomedin C, Bioassayable Growth- Promoting Activity (Thymidine Activity), and Transferrin in Human Fetuses: In Utero Study

Thiériot-Prévost

Daffos²,

Forestier³

et al. 1986

Pediatr Res

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ABSTRACI'. Serum somatomedin C, thymidine uptake stimulating activity, and transferrin were measured in fetal blood collected by ultrasound-guided puncture of umbilical vessels in utero during prenatal assessment for mother-tofetus transmissible infections. Serum somatomedin C and transferrin were measured by immunoassay. The role of growth factors in fetal development is not clear. Available information indicates that the levels of somatomedin/ IGF I and I1 in human fetal blood are low (1-3) while it has been reported that another factor measured as fetal brain radioreceptor assayable somatomedin is in high quantity (4). In previous studies we characterized a method to measure the growth-promoting activity of human serum by assessing the incorporation of tritiated thymidine into lectin-activated human lymphocytes (5, 6) and applied it to newborns (7). The availability of normal fetal blood collected in utero for purpose of prenatal diagnosis of infection provided the opportunity to extend the study to fetuses. Herein we report our results in fetal blood, in association with measurement of Sm C and transfenin. MATERIALS AND METHODSThe serum samples used in this study were obtained by direct puncture of the umbilical vessels in utero. Intrauterine cord blood sampling was performed to determine whether maternal rubella or toxoplasmic infection had involved the fetus. The ultrasoundguided technique and its results in the prenatal diagnosis of

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Low somatomedin activity in cord serum from infants with intrauterine growth retardation

Cited by 56 publications

References 25 publications

Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

Serum Insulin-Like Growth Factors and Insulin-Like Growth Factor Binding Proteins in the Human Fetus. Relationships with Growth in Normal Subjects and in Subjects with Intrauterine Growth Retardation

Serum Somatomedin C, Bioassayable Growth- Promoting Activity (Thymidine Activity), and Transferrin in Human Fetuses: In Utero Study

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