A prospective study of maternal serum insulin-like growth factor-I in pregnancies with appropriately grown or growth restricted fetuses (original) (raw)
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Early Human Development, 1997
A prospective observational study of 104 women was performed to study whether the insulin-like growth factor (IGF) system in pregnancy before labour is associated with reduced fetal growth. Fetal blood was obtained by cordocentesis for prenatal diagnosis or at elective caesarean delivery and a maternal sample was also obtained. IGF-1 and IGF-2 and their binding proteins -1 and -3 were measured by RIA. The 35 cases were smaller than -2S.D.s by ultrasound abdominal circumference and birthweight and were subdivided into fetal growth retardation (FGR, n = 20) and small for gestational age (SGA, n = 15) by Doppler velocimetry and neonatal outcome. Controls (n = 69) were normally grown.
Hormone Research in Paediatrics, 2007
Background: The maternal insulin-like growth factor (IGF) system is considered to be involved in fetal growth regulation. However, available data linking this system to fetal growth are contradictory and incomplete. Aims: To measure components of the IGF system before, during and after pregnancy in healthy women and to relate these results, and their changes during pregnancy, to fetal weight (gestational week 31) and birth weight. Methods: Serum concentrations of IGF-I, IGF-II, IGF-binding protein (IGFBP)-1, IGFBP-3 and IGFBP-3 protease activity were assessed in 23 women before conception, at weeks 8, 14, 20, 32 and 35 of pregnancy and 2 weeks postpartum. The data were analyzed using simple and multiple linear regression. Results: One third of the variability in fetal weight was explained by IGF-I in combination with IGFBP-3 protease activity, both assessed at gestational week 32 (p = 0.013). Birth weight was negatively correlated (r = –0.43 to –0.59) with IGFBP-1 at gestational wee...
Acta Histochemica, 2001
Many cases of intrauterine growth retardation (IUGR) are the result of placental and fetal tissue insufficiency. Insulin-like growth factor-I (IGF-I) is known to play a role in placental and fetal growth. An immunocytochemical study was performed to localize IGF-I peptides in human placenta and umbilical cords of normal (n = 3) and IUGR (n = 3) fetuses. The peripartum fetal conditions were evaluated as well. Immunoreactive IGF-I was detected in the cytotrophoblast, syncytiotrophoblast, amnion, endothelial cells of fetal capillaries and in the decidua in both normal and IUGR placental tissue. A more robust immunostaining and increased numbers of positively stained cells were found in the decidua of IUGR placenta (p < 0.001). Intense immunostaining was also found in endothelial cells, smooth muscle cells and fibroblasts of the umbilical vein. IGF-I immunoreactivity was also present in stroma (Hofbauer cells and/or fibroblasts) of IUGR villi. Our results indicate that expression of IGF-I is high in specific sites in placenta and umbilical cords, which indicates a paracrine and/or endocrine function. The increased expression of IGF-I in placenta of IUGR fetuses indicates its involvement in restoring normal growth by means of a positive feed-back mechanism.
Molecular Human Reproduction, 2001
Intrauterine growth restriction (IUGR) is generally defined as the pathological restriction of fetal growth resulting in a fetus with birth weight below the 10th percentile for gestational age. Almost 75% of IUGR cases develop during third trimester. Studies on animals (rodents and sheep) as well as humans suggest that insulin-like growth factor-I (IGF-I), under the influence of placental growth hormone (PGH) plays crucial roles in fetal growth regulation during this period. Limited data are available with regard to IGF-I and PGH in placentae of normal and IUGR births. Therefore, in the present study, IGF-I and PGH mRNA expression has been studied in term placentae of normal (n ⍧ 10) and IUGR (n ⍧ 15) births by in-situ hybridization procedure. Their expression was also studied in first (n ⍧ 5) and second (n ⍧ 5) trimester placentae obtained from elective termination of normal pregnancies. Both IGF-I and PGH expression were found to be higher in the first and second trimester placentae compared to term placentae in normal pregnancies. However, IUGR term placentae showed increased expression of both IGF-I and PGH mRNA in comparison with normal placentae. Various mechanisms leading to the increased transcription of IGF-I and PGH mRNA in IUGR placenta are discussed. This increased transcription perhaps occurs in response to the reduction in the fetal growth.
Maternal insulin-like growth factor binding protein-1, body mass index, and fetal growth
Archives of Disease in Childhood - Fetal and Neonatal Edition, 2000
Aim-To examine the hypothesis that the maternal insulin-like growth factor system may constrain fetal growth. Methods-A prospective observational study of maternal serum insulin-like growth factor binding protein-1 (IGFBP-1) and fetal growth was undertaken in neonates with birthweights below the 5th centile. They had been classified either as having fetal growth restriction (FGR) due to placental dysfunction (increased umbilical artery Doppler pulsatility index (PI); n = 25) or as being small for gestational age (SGA; normal umbilical artery PI, growth velocity and amniotic fluid; n = 27). Eighty nine controls had normal birthweights (5th-95th centile), umbilical artery PI, growth velocity, and amniotic fluid. IGFBP-1 was measured by radioimmunoassay. Results-Among the controls, there was no significant correlation between IGFBP-1 and birthweight after allowing for body mass index (BMI). Maternal BMI was high in FGR and after adjusting for this, IGFBP-1 was increased (109 ng/ml) compared with SGA babies (69 ng/ml) and controls (57 ng/ml) and correlated with the umbilical artery PI. Conclusions-Maternal IGFBP-1 is probably not part of normal placental function. Its increase in FGR could be the cause or consequence of impaired placental perfusion, but high IGFBP-1 concentrations might further reduce the availability of maternal IGF-I to the placenta. This could worsen placental function and so adversely aVect fetal growth.
2004
Objective: To determine serum levels of insulin-like growth factor-I, free insulin-like growth factor-I and its binding proteins in maternal serum and in cord blood of two groups of newborns with different birth weights. Methods: A group of 60 healthy pregnant women and their respective neonates with birth weight ≥ 2500g (group 1) and another comprising 23 healthy pregnant women and their respective neonates with birth weight ≤ 2500g (group 2) were studied. Maternal and neonatal blood samples were analyzed for levels of insulin-like growth factor-I, free insulin-like growth factor-I, binding protein-1 and binding protein-3 by radioimmunoassay. Statistical analysis: Student's t test and multiple regression analysis. Values of p < 0.05 were considered statistically significant. Results: The t test showed that maternal insulin-like growth factor-I, neonatal insulin-like growth factor-I, and neonatal binding protein-3 values were significantly higher in Group 1 than in Group 2. In both groups maternal values were higher than those of their neonates (p < 0.05). Multiple regression analysis showed a positive correlation between neonatal anthropometric variables and neonatal insulin-like growth factor-I. Maternal binding protein-1 showed a negative correlation with neonatal insulin-like growth factor-I and binding protein-3. There was a positive correlation between maternal insulin-like growth factor-I and neonatal ratio free insulin-like growth factor-I/total insulin-like growth factor-I. Conclusion: The findings of this study suggest that insulin-like growth factor-I and its binding proteins 1 and 3 play a role in the regulation of late fetal growth in normal Brazilian pregnant women.
Placental phenotype and the insulin-like growth factors: resource allocation to fetal growth
The Journal of Physiology, 2017
Bloomfield FH, van Zijl PL, Bauer MK & Harding JE. (2002b). A chronic low dose infusion of insulin-like growth factor I alters placental function but does not affect fetal growth. Reprodroduction, Fertility and Develpoment 14, 393-400. Bloxam DL, Bax BE & Bax CM. (1994). Epidermal growth factor and insulin-like growth factor I differently influence the directional accumulation and transfer of 2-aminoisobutyrate (AIB) by human placental trophoblast in two-sided culture. Biochemical and Biophysical Research Communications 199, 922-929.
Diabetes, Obesity and Metabolism, 2001
Aim: Fetal intrauterine growth retardation (IUGR) is one of the most common obstetric problems, with a frequency of 12% in Mexico. In the past, investigations have focused on extrinsic causes of IUGR. More recent studies have examined the intrinsic factors that cause fetal intrauterine growth. Maintenance of fetal growth has been attributed to insulin-like growth factor (IGF), epidermal growth factor (EGF) and transforming growth factor beta (TGF-b). The objective of this study was to assess the levels of these growth factors during pregnancy and to determine whether or not low concentrations are associated with IUGR. Methods: Nine women whose pregnancies were complicated by IUGR and a group of nine women whose pregnancies exhibited normal fetal intrauterine growth were studied. IUGR was determined by sonography and con®rmed by weight at birth. Venous blood samples were taken from both groups of pregnant women at the end of each trimester. Enzyme-linked immunosorbent assays, immunoradiometric assays and radioimmunoassays were used to process samples, and the results were analysed by ANOVA. Results: IGF-I levels increased in both groups during pregnancy, but the increase was lower (p < 0.001) in the IUGR group throughout pregnancy and at delivery. EGF did not show any signi®cant changes during pregnancy. Blood TGF-b levels varied only during the ®rst trimester of pregnancy. The differences were not statistically signi®cant. However, TGF-b concentrations were higher in the pregnancies with IUGR. Women in the IUGR group were smaller than in the control group (p < 0.05), and, using the covariance test (p < 0.05), this was found to be correlated with IGF-I levels but not with EGF or TGF-b levels. Conclusions: Changes in fetal weight might be explained by the different concentrations of IGF. The structural homology between IGF-1 and insulin could mean that the presence of higher levels of IGF would result in a increased energetic metabolism that could contribute to fetal growth. EGF levels were not related to IUGR, and TGF-b levels increased only during the ®rst 3 months in the IUGR group. This observation correlates with the in vitro action of TGF-b as a negative factor of growth, but as a positive support for sustaining early pregnancy. Our data illustrates that low height represents an increased risk factor for IUGR. These data also correlate with the studies involving extrinsic factors.
Maternal Insulin-Like Growth Factors-I and -II Act via Different Pathways to Promote Fetal Growth
Endocrinology, 2006
The placenta transports substrates and wastes between the maternal and fetal circulations. In mice, placental IGF-II is essential for normal placental development and function but, in other mammalian species, maternal circulating IGF-II is substantial and may contribute. Maternal circulating IGFs increase in early pregnancy, and early treatment of guinea pigs with either IGF-I or IGF-II increases placental and fetal weights