Insulin-like growth factor-binding protein-1 in umbilical artery and vein of term fetuses with signs suggestive of distress during labor

Verhaeghe, Johan; Billen, Jaak; Giudice, Linda C.

doi:10.1677/joe.0.1700585

Cited by 16 publications

(18 citation statements)

References 36 publications

(32 reference statements)

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“…It is known that Igfbp1 has an inhibitory role on Igf-stimulated growth and differentiation. In addition, IUGR caused by placental insufficiency and in utero hypoxia is associated with elevated levels of Igfbp1 (28,29). The underexpression of Igfbp1 in Slc7a7 Ϫ/Ϫ fetuses may simply reflect the inverse relationship between this binding protein and Igf1 (14).…”

Section: Discussionmentioning

confidence: 99%

Slc7a7 disruption causes fetal growth retardation by downregulating Igf1 in the mouse model of lysinuric protein intolerance

Sperandeo¹,

Annunziata²,

Bozzato³

et al. 2007

American Journal of Physiology-Cell Physiology

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The solute carrier family 7A member 7 gene (SLC7A7) encodes the light chain of the heterodimeric carrier responsible for cationic amino acid (CAA) transport across the basolateral membranes of epithelial cells in intestine and kidney. Mutations affecting SLC7A7 cause lysinuric protein intolerance (LPI), a multiorgan disorder with clinical symptoms that include visceromegaly, growth retardation, osteoporosis, hyperammonemia, and hyperdibasicaminoaciduria. Here, we describe the consequences of inactivating Slc7a7 in a mouse model of LPI. The Slc7a7 mutation was generated by high-throughput retroviral gene-trapping in embryonic stem cells. The Slc7a7(-/-) mouse displayed intrauterine growth restriction (IUGR), commonly leading to neonatal lethality. After heavy protein ingestion, the surviving adult animals presented metabolic derangement consistent with that observed in human LPI. IUGR was investigated by examining the expression of main factors controlling fetal growth. Insulin-like growth factor 1, the dominant fetal growth regulator in late gestation, was markedly downregulated as demonstrated by quantitative real-time RT-PCR, immunostaining and Western blot analysis in fetal liver. To further explore the pathophysiology of LPI, gene expression profiling analyses were carried out by DNA microarray technology in intestine and liver of adult Slc7a7(-/-) mice. Significant upregulation or downregulation (twofold or greater) was observed for 488 transcripts in intestine, and for 521 transcripts in the liver. The largest category of differentially expressed genes corresponds to those involved in transport according to Gene Ontology classification. This mouse model offers new insights into the pathophysiology of LPI and into mechanisms linking CAA metabolic pathways and growth control.

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Section: Discussionmentioning

confidence: 99%

Slc7a7 disruption causes fetal growth retardation by downregulating Igf1 in the mouse model of lysinuric protein intolerance

Sperandeo¹,

Annunziata²,

Bozzato³

et al. 2007

American Journal of Physiology-Cell Physiology

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“…The parents gave oral informed consent, and they were reassured that no DNA was to be extracted, and that the plasma sample would be discarded after completing the measurements described below. The current series contained no samples analyzed and reported on previously (2,3,15,22).…”

Section: Subjectsmentioning

confidence: 99%

“…IGFBP-1 acts as a growth-inhibitory factor (2,3), presumably because the formation of IGF-I:IGFBP-1 complexes reduces free IGF-I concentrations (4).…”

mentioning

confidence: 99%

Transient Catabolic State with Reduced IGF-I after Antenatal Glucocorticoids

et al. 2007

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Glucocorticoid (GC) administration before preterm birth reduces neonatal morbidity but may restrain growth. Here we explored the effect of antenatal GC on nutrient substrates [glucose, FFA, amino acids (AA)], and on IGF-I and IGF-binding protein-1 (IGFBP-1). We analyzed umbilical vein (UV) plasma obtained at birth from 91 preterm newborns that received one course of GC (last exposure 1-1358 h before birth) and 49 newborns that did not. We found that recent GC exposure (Յ48 h) raised glucose, FFA, and AA concentrations, and the homeostasis model assessment of insulin resistance (HOMA-IR) index, but lowered IGF-I concentrations. The AA surge was greater in newborns with a birth weight z score Ͻ0 than in those with a z score Ͼ0. Although all AA were transiently increased, the increment was most robust for glutamine and alanine. Shorter duration since GC administration and lower IGF-I concentrations independently predicted AA levels. In conclusion, an antenatal course of GC elicited a transient catabolic state encompassing all nutrient substrates, and a temporary drop in IGF-I concentrations. These changes may explain the growth-inhibitory effects of repeated antenatal GC administration. Future research should clarify the role of IGF-I in the protein-catabolic response to GC. (Pediatr Res 62: 295-300, 2007)

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“…In humans, birth weight is negatively correlated with IGFBP-1 concentrations in cord blood (11)(12)(13). In animal models of FGR, including uterine artery ligation, hypoxia, and maternal undernutrition, low birth weight is also associated with high circulating levels of IGFBP-1 as a result of increased production in the fetal liver (14 -20).…”

mentioning

confidence: 99%

Elevated Circulating Insulin-Like Growth Factor Binding Protein-1 Is Sufficient to Cause Fetal Growth Restriction

Watson¹,

Bialek²,

Anzo³

et al. 2006

Endocrinology

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IGF binding protein-1 (IGFBP-1) inhibits the mitogenic actions of the IGFs. Circulating IGFBP-1 is elevated in newborns and experimental animals with fetal growth restriction (FGR). To establish a causal relationship between high circulating IGFBP-1 and FGR, we have generated transgenic mice using the mouse alpha-fetoprotein gene promoter to target overexpression of human IGFBP-1 (hIGFBP-1) in the fetal liver. These transgenic mice (AFP-BP1) expressed hIGFBP-1 mainly in the fetal hepatocytes, starting at embryonic d 14.5 (E14.5), with lower levels in the gut. The expression peaked at 1 wk postnatally (plasma concentration, 474 +/- 34 ng/ml). At birth, AFP-BP1 pups were 18% smaller [weighed 1.34 +/- 0.02 g compared with 1.62 +/- 0.04 g for wild type (WT); P < 0.05], and they did not demonstrate any postnatal catch-up growth. The placentas of the AFP-BP1 mice were larger than WT from E16.5 onwards (150 +/- 12 for AFP-BP1 vs. 100 +/- 5 mg for WT at E16.5; P < 0.05). Thus, this model of FGR is associated with a larger placenta, but without postnatal catch-up growth. Overall, these data clearly demonstrate that high concentrations of circulating IGFBP-1 are sufficient to cause FGR.

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Insulin-like growth factor-binding protein-1 in umbilical artery and vein of term fetuses with signs suggestive of distress during labor

Cited by 16 publications

References 36 publications

Slc7a7 disruption causes fetal growth retardation by downregulating Igf1 in the mouse model of lysinuric protein intolerance

Slc7a7 disruption causes fetal growth retardation by downregulating Igf1 in the mouse model of lysinuric protein intolerance

Transient Catabolic State with Reduced IGF-I after Antenatal Glucocorticoids

Elevated Circulating Insulin-Like Growth Factor Binding Protein-1 Is Sufficient to Cause Fetal Growth Restriction

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