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      Longitudinal Study of the Maternal Insulin-Like Growth Factor System before, during and after Pregnancy in Relation to Fetal and Infant Weight

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          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 week 20 (p = 0.041), 32 (p = 0.012) and 35 (p = 0.003). Conclusion: We propose there is a finely tuned balance among the components of the IGF system, providing a means for fetal growth regulation.

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          Most cited references 17

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          Insulin-like growth factors and their binding proteins: biological actions

           J Jones (1995)
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            Intrauterine growth restriction in humans is associated with abnormalities in placental insulin-like growth factor signaling.

            The IGFs promote the growth and development of the feto-placental unit during gestation, and impairment of their placental actions may result in altered intrauterine growth of the fetus. In this study, proteins involved in IGF signaling were investigated in human placentas from pregnancies complicated by intrauterine growth restriction (IUGR) compared with those from normal pregnancies. IUGR placentas exhibited 33% reduction in the protein content of IGF-I receptors, but no changes in insulin receptor protein levels. In addition, insulin receptor substrate-2 (IRS-2) protein levels were reduced in IUGR placentas, with no changes in IRS-1 or Shc protein content, and this was associated with a parallel decrease in IRS-2-associated phosphatidyl inositol 3-kinase. Akt protein expression was also reduced in IUGR, whereas phosphorylation of Akt and its substrate glycogen synthase kinase-3 was unchanged. Finally, in IUGR placentas there was impaired activation of multiple members of the MAPK family, because phosphorylation of p38 and c-Jun N-terminal kinase was reduced 70%. In conclusion, human placentas from pregnancies complicated by IUGR are characterized by decreased IGF-I receptor content, selective impairment of the IRS-2/ phosphatidyl inositol 3-kinase pathway, and reduced p38 and c-Jun N-terminal kinase activation. The observed abnormalities in IGF-I signaling may contribute to altered fetal growth and development in human IUGR.
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              Regulation of Maternal Metabolism by Pituitary and Placental Hormones: Roles in Fetal Development and Metabolic Programming

               M Freemark (2006)
              This review outlines the regulation of maternal metabolism by hormones, cytokines and growth factors, highlighting recent studies that implicate disordered somatolactogen signalling in the pathogenesis of perinatal growth failure and the development of the metabolic syndrome.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                January 2008
                05 December 2007
                : 69
                : 2
                : 99-106
                aDepartment of Biomedicine and Surgery, Division of Nutrition, Linköping University, Linköping, and bUnit for Endocrinology and Diabetes, Karolinska Institutet, Department of Molecular Medicine, Karolinska Hospital M1:02, Stockholm, Sweden
                111813 Horm Res 2008;69:99–106
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 4, References: 28, Pages: 8
                Original Paper


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