Insulin-like Growth Factor I, Epidermal Growth Factor and Transforming Growth Factor Beta Expression and Their Association With Intrauterine Fetal Growth Retardation, Such as Development During Human Pregnancy

Diabetes Obes Metab. 2001 Dec;3(6):457-62. doi: 10.1046/j.1463-1326.2001.00168.x.

Abstract

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-beta). 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 confirmed 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 significant changes during pregnancy. Blood TGF-beta levels varied only during the first trimester of pregnancy. The differences were not statistically significant. However, TGF-beta 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-beta 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-beta levels increased only during the first 3 months in the IUGR group. This observation correlates with the in vitro action of TGF-beta 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Body Weight
  • Embryonic and Fetal Development / physiology*
  • Epidermal Growth Factor / genetics*
  • Female
  • Fetal Growth Retardation / physiopathology*
  • Gene Expression Regulation, Developmental
  • Humans
  • Infant, Newborn
  • Insulin-Like Growth Factor I / genetics*
  • Mexico
  • Pregnancy
  • Pregnancy Trimester, First
  • Pregnancy Trimester, Second
  • Pregnancy Trimester, Third
  • Socioeconomic Factors
  • Transforming Growth Factor beta / genetics*

Substances

  • Transforming Growth Factor beta
  • Epidermal Growth Factor
  • Insulin-Like Growth Factor I