Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

Prins, Frans A.; Hill, David J.; Fekete, M.; Robsen, D J; Fieller, Nick; Assche, F.A. Van; Milner, R. D. G.

doi:10.1203/00006450-198411000-00009

Cited by 23 publications

(14 citation statements)

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“…Fetuses from the UA-lig horns were growth retarded compared with pups from the opposite UA-nonlig uterine horn and compared with nonop control pups. As noted by other investigators (19), the greatest decrease in weight was at positions closest to the vascular disruption (position and body weight correlation, r = 0.704, p < 0.05). CRL was not different in the UA-nonlig and nonop animals but was decreased in pups from the UA-lig uterine horn compared with the UA-nonlig side, with the greatest decrease noted in animals nearest the ligated artery (UA-lig group, CRL, and position, r = 0.53 1, p < 0.05).…”

Section: Effect Of Ual On Fetal Survival Growth and Organ Weightsupporting

confidence: 51%

Changes in IGF-I and -II, IGF Binding Protein, and IGF Receptor Transcript Abundance after Uterine Artery Ligation

Price

Stiles

et al. 1992

Pediatr Res

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ABSTRACT. Altered IGF activity may be one mechanism IGF-I and -11 are synthesized in multiple fetal tissues and are involved in the pathogenesis of intrauterine growth retar-thought to participate in the autocrine/paracrine stimulation of dation (IUGR). We assessed the expression of IGF, IGF cellular proliferation and differentiation during development (1). binding protein (IGFBP), and IGF receptor transcripts in Decreased IGF action has been implicated in the pathophysiolliver, carcass, and placenta of fetal rats with IUGR result-ogy of fetal growth retardation resulting from a number of ing from unilateral uterine artery ligation. We found that etiologies. In man, IUGR has been associated with a reduction uterine artery ligation on d 17 of gestation resulted in in serum concentrations of immunoreactive IGF-I and IGF reduced body weight, liver weight, and placental weight on bioactivity (1). Animal models of IUGR caused by a decrease in d 20 in the fetuses from the ligated uterine horn (UA-lig) fetal nutrient intake also demonstrate decreased fetal serum compared with those from the opposite, nonligated uterine immunoreactive IGF-I and IGF bioactivity (2-5). A potential horn (UA-nonlig) and those from dams with no surgery or mechanism for the alterations in IGF bioactivity might include anesthesia. As assessed by solution hybridization, UA-lig changes in IGFBP expression. fetuses exhibited significantly higher hepatic IGFBP-1, Six IGFBP have been identified and characterized thus far IGFBP-2, and IGF-I1 transcript abundance than UA-non-(IGFBP 1-6) (6-1 1). In many situations; IGFBP appear to lig controls (increased 110,50, and 31%, respectively). The decrease IGF activity by sequestering free' IGF in serum (12). only major difference among groups in carcass and placenta IGFBP also may modulate IGF activity by altering the interacmRNA abundance was a 44% decrease in placental IGF-tion between the IGF and the type 1 IGF receptor at the cell I1 expression in UA-lig pups compared with pups from surface, thereby either inhibiting or augmenting IGF actions dams that had had no surgery or anesthesia. Serum (13). Moreover, IGFBP appear to be regulated in a tissue-specific IGFBP, analyzed by ligand blot, showed a 2.4-fold increase fashion (14, 15) and may participate in the local regulation of in the doublet IGFBP-11-2 band in UA-lig fetuses. Serum organ growth. For example, we found an increase in liver and immunoreactive IGFBP-2 was unchanged among the lung IGFBP-1 mRNA in growth-retarded fetal rats after maternal groups, indicating that IGFBP-1 accounted for the increase dexamethasone administration (16). Increased local expression in doublet intensity. Our results suggest that increased of IGFBP-1 could account for the marked organ growth retarserum IGFBP-1 concentrations may decrease IGF activity dation found in this model in serum and thus inhibit IGF-stimulated cell proliferation UAL provides a model of uteroplacental insufficiency and the or, by crossing the endothelial border, inhibit the activity IUGR that res...

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Section: Effect Of Ual On Fetal Survival Growth and Organ Weightsupporting

confidence: 51%

Changes in IGF-I and -II, IGF Binding Protein, and IGF Receptor Transcript Abundance after Uterine Artery Ligation

Price

Stiles

et al. 1992

Pediatr Res

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“…Unlike the original report of Wigglesworth (12) and this study, DePrins et ul. (21) did not find that fetal size was influenced by the proximity of the conceptus to the site of uterine artery ligation. Subtle differences in techniques may explain this discrepancy.…”

Section: Discussionmentioning

confidence: 93%

Tissue and Serum Concentrations of Somatomedin-C/Insulin-Like Growth Factor I in Fetal Rats Made Growth Retarded by Uterine Artery Ligation

Vileisis

D’Ercole

1986

Pediatr Res

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“…IUGR in rats, induced either by maternal fasting (70), maternal diabetes (71), or restricted uteroplacental blood flow (72), is associated with reduced circulating IGF levels, pancreatic weights, and pancreatic insulin contents. Parallel findings exist in human infants following IUGR (73).…”

Section: Abnormal Expression Of Transcription and Growth Factors Leadmentioning

confidence: 99%

Pancreatic Development and Adult Diabetes

Hill

Duvillié

2000

Pediatr Res

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Low birth weight is an important risk factor for type 2 diabetes in later life. Maturity-onset diabetes of the young has been linked to genetic sequence abnormalities in transcription factors known to be involved in endocrine pancreatic development. These observations suggest that both the maternal environment and the fetal genome can influence the number and/or function of pancreatic ␤ cells in early life, and that this has life-long implications for postnatal diabetes. This article reviews the evidence that suggests that ␤ cells derive from a neogenic process within the pancreatic ductal epithelium, controlled by specific transcription factors and locally acting peptide growth factors. In rodents, many of the fetal phenotypes of ␤ cells are destroyed during neonatal life in a developmental apoptosis and are replaced by a second wave of neogenesis. This results in islets with insulin release characteristics suited to postnatal life. The timing and amplitude of these ontological events are altered by nutritional sufficiency, and this may be mediated by changes in pancreatic growth factor expression, particularly of the IGF axis. Because ␤-cell plasticity after the perinatal period is limited, a dysfunctional programming of ␤-cell ontogeny may present a long-term risk factor for glucose intolerance and type 2 diabetes. This critical window of pancreatic development is likely to occur in third trimester of human development. Abbreviations MODY, maturity-onset diabetes of the young IUGR, intrauterine growth restriction Shh, Sonic hedgehog gene PP, pancreatic peptide FGF, fibroblast growth factor DTA, diphtheria toxin HNF, hepatocyte nuclear factor PTF1, pancreatic transcription factor 1 VEGF, vascular endothelial growth factor INTRAUTERINE GROWTH RESTRICTION AND GLUCOSE HOMEOSTASIS IN ADULTSIUGR is a risk factor for both perinatal disease and diseases of later life. Barker et al. showed that a strong inverse correlation exists between mortality from cardiovascular disease below age 65 and birth weight (1). Similarly, the relative risk for prevalence of syndrome X, consisting of type 2 diabetes, hypertension and hyperlipidemia, is 18-fold higher in males born Ͻ2.5 kg compared with those Ͼ4 kg (1, 2). The at-risk individuals were thin at birth with a low ponderal index. Impaired glucose tolerance can be detected as early as 7 y of age in children who at birth had low weight and were thin (3). This implies that a programming of the metabolic axis can occur in early life, which is modulated by the intrauterine environment. For type 2 diabetes this may result from an altered development and insulin-secreting capacity of the endocrine pancreas, or by altered insulin sensitivity of target tissues. It is possible that perturbations of prenatal growth may lead to inappropriate ␤-cell ontogeny and result in a population of ␤ cells qualitatively ill suited to subsequently manage metabolic stress. A reduced availability of insulin prenatally is a major contributor to IUGR. This can be experimentally demonstrated in extreme for...

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Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

Cited by 23 publications

References 29 publications

Changes in IGF-I and -II, IGF Binding Protein, and IGF Receptor Transcript Abundance after Uterine Artery Ligation

Changes in IGF-I and -II, IGF Binding Protein, and IGF Receptor Transcript Abundance after Uterine Artery Ligation

Tissue and Serum Concentrations of Somatomedin-C/Insulin-Like Growth Factor I in Fetal Rats Made Growth Retarded by Uterine Artery Ligation

Pancreatic Development and Adult Diabetes

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