Expression of Messenger RNA of Insulin-Like Growth Factors (IGFs) and IGF Binding Proteins (IGFBP1-6) in Placenta of Normal and Diabetic Pregnancy.

Liu, Yanjun; Tsushima, Takahiro; Onoda, Noritaka; Minei, Satomi; Sanaka, Mayumi; Nagashima, Tamaki; Yanagisawa, Keiji; Omori, Yasue

doi:10.1507/endocrj.43.suppl_s89

Cited by 31 publications

(4 citation statements)

References 10 publications

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“…We have observed that IGF-BP3 levels are increased in the serum of GDM mothers and their macrosomic infants and IGF-I levels were significant correlated with IGF-BP3 in macrosomic newborns ( r = 0.36, n = 30, P = 0.04). Our observations are in close agreement with the results of several investigators [29] who have demonstrated an increase in cord serum IGF-BP3 concentrations in GDM pregnancies, though Hill et al [23] have observed no significant modifications in the levels of IGF-BP3 of GDM mothers and their babies. In our study, the high levels of IGF-BP3 in GDM and their macrosomic infants are not contributed by the placenta as the IGF-BP3 mRNA expression is downregulated in GDM women.…”

Section: Discussionsupporting

confidence: 93%

Growth factor concentrations and their placental mRNA expression are modulated in gestational diabetes mellitus: possible interactions with macrosomia

Grissa

Yessoufou

Mrisak

et al. 2010

BMC Pregnancy Childbirth

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BackgroundGestational diabetes mellitus (GDM) is a form of diabetes that occurs during pregnancy. GDM is a well known risk factor for foetal overgrowth, termed macrosomia which is influenced by maternal hypergycemia and endocrine status through placental circulation. The study was undertaken to investigate the implication of growth factors and their receptors in GDM and macrosomia, and to discuss the role of the materno-foeto-placental axis in the in-utero regulation of foetal growth.Methods30 women with GDM and their 30 macrosomic babies (4.75 ± 0.15 kg), and 30 healthy age-matched pregnant women and their 30 newborns (3.50 ± 0.10 kg) were recruited in the present study. Serum concentrations of GH and growth factors, i.e., IGF-I, IGF-BP3, FGF-2, EGF and PDGF-B were determined by ELISA. The expression of mRNA encoding for GH, IGF-I, IGF-BP3, FGF-2, PDGF-B and EGF, and their receptors, i.e., GHR, IGF-IR, FGF-2R, EGFR and PDGFR-β were quantified by using RT-qPCR.ResultsThe serum concentrations of IGF-I, IGF-BP3, EGF, FGF-2 and PDGF-B were higher in GDM women and their macrosomic babies as compared to their respective controls. The placental mRNA expression of the growth factors was either upregulated (FGF-2 or PDGF-B) or remained unaltered (IGF-I and EGF) in the placenta of GDM women. The mRNA expression of three growth factor receptors, i.e., IGF-IR, EGFR and PDGFR-β, was upregulated in the placenta of GDM women. Interestingly, serum concentrations of GH were downregulated in the GDM women and their macrosomic offspring. Besides, the expression of mRNAs encoding for GHR was higher, but that encoding for GH was lower, in the placenta of GDM women than control women.ConclusionsOur results demonstrate that growth factors might be implicated in GDM and, in part, in the pathology of macrosomia via materno-foeto-placental axis.

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Section: Discussionsupporting

confidence: 93%

Growth factor concentrations and their placental mRNA expression are modulated in gestational diabetes mellitus: possible interactions with macrosomia

Grissa

Yessoufou

Mrisak

et al. 2010

BMC Pregnancy Childbirth

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“…Their lack of hyperglycemia may partly explain the absence of late macrosomia. Macrosomia has been observed in 10-27% of human fetuses exposed to maternal diabetes (25) and has been associated with the following: maternal hyperglycemia (26), fetal hyperinsulinemia (25), and increased insulin-like growth factors in neonates (20). Therefore, GLUT1 deficiency does not appear to explain late gestational macrosomia in the offspring of diabetic mothers, although it does impair early embryonic growth.…”

Section: Discussionmentioning

confidence: 99%

Glucose transporter-1-deficient mice exhibit impaired development and deformities that are similar to diabetic embryopathy

Heilig

Saunders

Brosius

et al. 2003

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

106

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The hyperglycemia of maternal diabetes suppresses the glucose transporter-1 (GLUT1) facilitative glucose transporter 49 -66% in preimplantation embryos. Glucose uptake is reduced and apoptosis is activated. We hypothesized that the reduction of embryonic GLUT1 may play a key role in the malformations of diabetic embryopathy. Therefore, we produced GLUT1-deficient transgenic mice [i.e., antisense-GLUT1 (GT1AS)] to determine whether GLUT1 deficiency alone could reproduce the growth defects. Early cell division of fertilized mouse eggs injected with GT1AS was markedly impaired, P < 0.001 vs. controls. Two populations of preimplantation embryos obtained from GT1AS ؋ GT1AS heterozygote matings exhibited reduction of the 2-deoxyglucose uptake rate: one by 50% (presumed heterozygotes, P < 0.001 vs. control) and the other by 95% (presumed homozygotes, P < 0.001 vs. heterozygotes). Embryonic GLUT1 deficiency in the range reported with maternal diabetes was associated with growth retardation and developmental malformations similar to those described in diabetes-exposed embryos: intrauterine growth retardation (31.1%), caudal regression (9.8%), anencephaly with absence of the head (6.6%), microphthalmia (4.9%), and micrognathia (1.6%). Reduced body weight (small embryos, <70% of the nontransgenic body weight) was accompanied by other malformations and a 56% reduction of GLUT1 protein, P < 0.001 vs. nonsmall embryos (body weight >70% normal). The heart, brain, and kidneys of embryonic day 18.5 GT1AS embryos exhibited 24 -51% reductions of GLUT1 protein. The homozygous GT1AS genotype was lethal during gestation. Reduced embryonic GLUT1 was associated with the appearance of apoptosis. Therefore, GLUT1 deficiency may play a role in producing embryonic malformations resulting from the hyperglycemia of maternal diabetes. Late gestational macrosomia was absent, apparently requiring a different mechanism.embryo ͉ antisense ͉ transgenic ͉ development ͉ apoptosis

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“…However, one study found sex-specific variation in cord blood IGF-1 in infants of diabetic mothers [ 286 ]: male infants had higher cord blood IGF-2, IGFBP-3, c -peptide and leptin and lower IGF-1 adjusted for IGFBP-3 [ 286 ], while female infants had higher cord blood IGF-1 adjusted for IGFBP-3 ( Table 3 ) without significant differences in other hormone levels [ 286 ]. Several additional studies found elevated cord blood IGF-2 levels in infants born to mothers with gestational diabetes, but sex differences were not analyzed [ 118 , 289 , 290 ].…”

Section: Effects Of Maternal Disorders On Fetal Hormones Growth Facto...mentioning

confidence: 99%

Hormonal Determinants of Growth and Weight Gain in the Human Fetus and Preterm Infant

Page,

Younge,

Freemark

2023

Nutrients

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The factors controlling linear growth and weight gain in the human fetus and newborn infant are poorly understood. We review here the changes in linear growth, weight gain, lean body mass, and fat mass during mid- and late gestation and the early postnatal period in the context of changes in the secretion and action of maternal, placental, fetal, and neonatal hormones, growth factors, and adipocytokines. We assess the effects of hormonal determinants on placental nutrient delivery and the impact of preterm delivery on hormone expression and postnatal growth and metabolic function. We then discuss the effects of various maternal disorders and nutritional and pharmacologic interventions on fetal and perinatal hormone and growth factor production, growth, and fat deposition and consider important unresolved questions in the field.

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Expression of Messenger RNA of Insulin-Like Growth Factors (IGFs) and IGF Binding Proteins (IGFBP1-6) in Placenta of Normal and Diabetic Pregnancy.

Cited by 31 publications

References 10 publications

Growth factor concentrations and their placental mRNA expression are modulated in gestational diabetes mellitus: possible interactions with macrosomia

Growth factor concentrations and their placental mRNA expression are modulated in gestational diabetes mellitus: possible interactions with macrosomia

Glucose transporter-1-deficient mice exhibit impaired development and deformities that are similar to diabetic embryopathy

Hormonal Determinants of Growth and Weight Gain in the Human Fetus and Preterm Infant

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