Circulating insulin-like growth factor I levels in newborn premature and full-term infants followed longitudinally

Lineham, Jennifer D.; Smith, Richard M.; Dahlenburg, G. W.; King, R. W.; Haslam, Ross; Stuart, Margaret C.; Faull, Linda

doi:10.1016/0378-3782(86)90096-4

Cited by 82 publications

(66 citation statements)

References 18 publications

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“…A key difference between vascular growth in utero and after birth is that IGF-I falls in premature infants after birth (16). Our findings suggest that if IGF-I increases quickly in premature infants after delivery, allowing normal vascular development, ROP does not occur.…”

Section: Discussionmentioning

confidence: 67%

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Low IGF-I suppresses VEGF-survival signaling in retinal endothelial cells: Direct correlation with clinical retinopathy of prematurity

Hellström¹,

Perruzzi²,

Ju³

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

533

403

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Retinopathy of prematurity is a blinding disease, initiated by lack of retinal vascular growth after premature birth. We show that lack of insulin-like growth factor I (IGF-I) in knockout mice prevents normal retinal vascular growth, despite the presence of vascular endothelial growth factor, important to vessel development. In vitro, low levels of IGF-I prevent vascular endothelial growth factor-induced activation of protein kinase B (Akt), a kinase critical for endothelial cell survival. Our results from studies in premature infants suggest that if the IGF-I level is sufficient after birth, normal vessel development occurs and retinopathy of prematurity does not develop. When IGF-I is persistently low, vessels cease to grow, maturing avascular retina becomes hypoxic and vascular endothelial growth factor accumulates in the vitreous. As IGF-I increases to a critical level, retinal neovascularization is triggered. These data indicate that serum IGF-I levels in premature infants can predict which infants will develop retinopathy of prematurity and further suggests that early restoration of IGF-I in premature infants to normal levels could prevent this disease.

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Section: Discussionmentioning

confidence: 67%

“…IGF-I is an important somatic growth factor that is correlated with birth weight (14,15) and gestational age (16,17). In particular, IGF-I is not maintained at in utero levels after premature birth (16) perhaps because of loss of IGF-I sources from placenta and from amniotic fluid that is ingested by the fetus.…”

mentioning

confidence: 99%

Low IGF-I suppresses VEGF-survival signaling in retinal endothelial cells: Direct correlation with clinical retinopathy of prematurity

Hellström¹,

Perruzzi²,

Ju³

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

533

403

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show abstract

“…[28][29][30][31][32][33] In the third trimester of pregnancy, fetal insulin like growth factor-1 (IGF-1) levels rise rapidly in utero 36 and then fall precipitously from in utero levels after premature birth. 37 Insulin like growth factor-1 is consequently low after preterm birth and is in fact initially lowest in those who later develop ROP. 38, 39 The action of VEGF is dependent on IGF-1, which is transported across the placenta.…”

Section: 33mentioning

confidence: 99%

Oxygen and retinopathy of prematurity

Saugstad

2006

J Perinatol

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Retinopathy of prematurity is on the rise and a third epidemic has been identified. In spite of extensive research and progress in the understanding of this disease in recent years, 50 000 children worldwide are blinded by this condition each year. The relation between hyperoxia, low-gestational age, growth retardation, oxygen dependent growth factors, and oxidative stress are now being understood more clearly. We know that in the first phase of retinopathy of prematurity, hyperoxia inhibits vascular endothelial growth factor. In the second phase, vascular endothelial growth factor rises, and when insulin-like growth factor-1 reaches a threshold around 32 to 34 weeks postconceptional age, uncontrolled neovascularization may occur. It is not known whether this new knowledge will have implications for future therapy. However, by strictly avoiding hyperoxia, that is, SaO 2 >92-93% and avoiding fluctuations in SaO 2 , it is possible to control and prevent severe retinopathy of prematurity in most cases.

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“…IGFBP-3 can exhibit either an inhibitory (4) or a potentiating (5) effect on IGF-I bioactivity in vitro, depending on its ability to alter the equilibrium between IGF-I and its receptor (5). Although IGF-I is thought to play an important role in postnatal growth (6)(7)(8)(9)(10)(11)(12)(13)(14)(15), there is disagreement among authors (16)(17)(18)(19) about the effects of postnatal age on plasma IGF-I in early infancy. The usefulness of obtaining plasma IGF-I concentrations in infancy is limited because normal values for this age group have not been established.…”

mentioning

confidence: 99%

“…The usefulness of obtaining plasma IGF-I concentrations in infancy is limited because normal values for this age group have not been established. Data on the circulating IGF-I concentrations in healthy term infants in early infancy are available from only five published reports (10,(16)(17)(18)(19). These studies were either cross-sectional (10,16,17) or followed a relatively small number of infants longitudinally (16)(17)(18)(19).…”

mentioning

confidence: 99%

Insulin-Like Growth Factor (IGF)-I and IGF-Binding Protein 3 during the First Year in Term and Preterm Infants

et al. 1995

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Plasma IGF-I and IGF-binding protein 3 (IGFBP-3) were determined by radioimmunoassay in term infants (n = 51) at 0, 2,4, 6, and 12 mo and preterm infants (n = 51) at -3 (28.4 wk postconceptional age), -2, -1.5, -1,0,2,4,6,9, and 12 rna from expected term. The effects of gestational age at birth (term or preterm) and study age were determined by repeated measures analysis of variance and Fisher's least squares difference. In preterm infants, IGF-I increased between -3 and 2 mo from 0.75 to 10.4 nM, decreased between 2 and 9 mo to 7.3 nM, and increased again between 9 and 12 mo to 10.1 nM (p < 0.0001), whereas IGFBP-3 increased relatively little from -3 to 0 rna (14.2 to 30.2 nM, p < 0.05) and plateaued from 2 to 12 mo (49.8 to 62.3 nM). At 0 rna, IGF-I and IGFBP-3 were the same in term and preterm infants, but preterm infants had higher IGF-I from 2 IGF mediate the growth-promoting actions of growth hormone in regulating the proliferation and differentiation of different cell types (1). These polypeptides which are structurally homologous to insulin also exert insulin-like metabolic effects. Both these effects are mediated through target cell surface receptors (2). Most tissues in the body produce IGF, and they are present in serum mostly bound to specific high molecular weight binding proteins (3). Of the six IGFBP that have been identified so far, IGFBP-3 is the major form present in the serum (1, 2) and demonstrates a high affinity for both IGF-I and IGF-II. IGFBP-3 can exhibit either an inhibitory (4) or a potentiating (5) effect on IGF-I bioactivity in vitro, depending on its ability to alter the equilibrium between IGF-I and its receptor (5).

show abstract

Circulating insulin-like growth factor I levels in newborn premature and full-term infants followed longitudinally

Cited by 82 publications

References 18 publications

Low IGF-I suppresses VEGF-survival signaling in retinal endothelial cells: Direct correlation with clinical retinopathy of prematurity

Low IGF-I suppresses VEGF-survival signaling in retinal endothelial cells: Direct correlation with clinical retinopathy of prematurity

Oxygen and retinopathy of prematurity

Insulin-Like Growth Factor (IGF)-I and IGF-Binding Protein 3 during the First Year in Term and Preterm Infants

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