Alterations in postnatal growth and metabolism following prenatal treatment of intrauterine growth restriction with Ad.VEGF gene therapy in the sheep

2011 ◽  
Vol 96 (Supplement 1) ◽  
pp. Fa7-Fa7 ◽  
Author(s):  
D. J. Carr ◽  
R. P. Aitken ◽  
J. S. Milne ◽  
D. M. Peebles ◽  
I. Zachary ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Intrauterine Growth Restriction ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Prenatal Treatment ◽  
Intrauterine Growth

scholarly journals Postnatal Growth after Intrauterine Growth Restriction Alters Central Leptin Signal and Energy Homeostasis

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30616 ◽  
Author(s):  
Bérengère Coupé ◽  
Isabelle Grit ◽  
Philippe Hulin ◽  
Gwenaëlle Randuineau ◽  
Patricia Parnet
Keyword(s):  
Intrauterine Growth Restriction ◽  
Energy Homeostasis ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Intrauterine Growth

scholarly journals Prenatal intrauterine growth restriction and risk of retinopathy of prematurity

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Alison Chu ◽  
Yasmeen Dhindsa ◽  
Myung Shin Sim ◽  
Marie Altendahl ◽  
Irena Tsui
Keyword(s):  
Gestational Age ◽  
Retinopathy Of Prematurity ◽  
Intrauterine Growth Restriction ◽  
Growth Failure ◽  
Postnatal Growth ◽  
Growth Patterns ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Prenatal Growth ◽  
Postnatal Growth Failure

Abstract Low birthweight and decreased postnatal weight gain are known predictors of worse retinopathy of prematurity (ROP) but the role of prenatal growth patterns in ROP remains inconclusive. To distinguish small for gestational age (SGA) from intrauterine growth restriction (IUGR) as independent predictors of ROP, we performed a retrospective cohort study of patients who received ROP screening examinations at a level IV neonatal intensive care unit over a 7-year period. Data on IUGR and SGA status, worst stage of and need for treatment for ROP, and postnatal growth was obtained. 343 infants were included for analysis (mean gestational age = 28.6 weeks and birth weight = 1138.2 g). IUGR infants were more likely to have a worse stage of ROP and treatment-requiring ROP (both p < 0.0001) compared to non-IUGR infants. IUGR infants were more likely to be older at worst stage of ROP (p < 0.0001) and to develop postnatal growth failure (p = 0.01) than non-IUGR infants. Independent of postnatal growth failure status, IUGR infants had a 4–5 × increased risk of needing ROP treatment (p < 0.001) compared to non-IUGR infants. SGA versus appropriate for gestational age infants did not demonstrate differences in retinopathy outcomes, age at worst ROP stage, or postnatal growth failure. These findings emphasize the importance of prenatal growth on ROP development.

scholarly journals Intraplacental Gene Therapy with Ad-IGF-1 Corrects Naturally Occurring Rabbit Model of Intrauterine Growth Restriction

2015 ◽  
Vol 26 (3) ◽  
pp. 172-182 ◽  
Author(s):  
Sundeep G. Keswani ◽  
Swathi Balaji ◽  
Anna B. Katz ◽  
Alice King ◽  
Khaled Omar ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Intrauterine Growth Restriction ◽  
Rabbit Model ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Naturally Occurring

scholarly journals Effect of intrauterine growth restriction on weight and cellularity of gastrointestinal tract in postnatal lambs

2008 ◽  
Vol 88 (1) ◽  
pp. 107-112 ◽  
Author(s):  
Feng Gao ◽  
Xianzhi Hou ◽  
Yingchun Liu
Keyword(s):  
Gastrointestinal Tract ◽  
Dna Content ◽  
Intrauterine Growth Restriction ◽  
Late Pregnancy ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Control Group ◽  
Intrauterine Growth ◽  
Significant Difference ◽  
Restricted Group

This study investigated the effect of intrauterine growth restriction (IUGR) during late pregnancy on weight and cellularity of the gastrointestinal tract (GIT) in postnatal lambs. Twenty-three Mongolian lambs were entered into the study. Their dams were mated at a synchronized estrus and divided into three groups offered 0.175 MJ ME kg-0.75 d-1 (Restricted Group 1, RG1), 0.33 MJ ME kg-0.75 d-1 (Restricted Group 2, RG2) and Control Group (CG, ad libitum access to feed) during their late pregnancy (90 d), respectively. The lambs were slaughtered at birth (neonatal lambs) and at 28 wk of age. The neonatal abomasum weight, jejunum weight and length, abomasum and jejunum DNA content, and the reticulum protein:DNA ratio were lower for RG1 than those of CG (P < 0.05). At 28 wk of age, there were no significant difference in the weights and lengths of jejunum and the weight of abomasum in the lambs among RG1, RG2 and CG (P > 0.05). However, the rumen and omasum weight, and omasum DNA content were lower for RG1 than for CG (P < 0.05). For the jejunum, the protein:DNA ratios in RG2 were significantly higher than those of CG (P < 0.05). These changes in the weight and cellularity of the GIT may have significant implications on postnatal growth and health. Key words: Intrauterine growth restriction, postnatal lambs, gastrointestinal tract, weight, cellularity

scholarly journals Intrauterine Growth Restriction: New Insight from the Metabolomic Approach

Metabolites ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 267 ◽  
Author(s):  
Elena Priante ◽  
Giovanna Verlato ◽  
Giuseppe Giordano ◽  
Matteo Stocchero ◽  
Silvia Visentin ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Clinical Aspects ◽  
Intrauterine Growth ◽  
Thrifty Phenotype ◽  
Thrifty Phenotype Hypothesis ◽  
Uterine Environment ◽  
Short And Long Term

Recognizing intrauterine growth restriction (IUGR) is a matter of great concern because this condition can significantly affect the newborn’s short- and long-term health. Ever since the first suggestion of the “thrifty phenotype hypothesis” in the last decade of the 20th century, a number of studies have confirmed the association between low birth weight and cardiometabolic syndrome later in life. During intrauterine life, the growth-restricted fetus makes a number of hemodynamic, metabolic, and hormonal adjustments to cope with the adverse uterine environment, and these changes may become permanent and irreversible. Despite advances in our knowledge of IUGR newborns, biomarkers capable of identifying this condition early on, and stratifying its severity both pre- and postnatally, are still lacking. We are also still unsure about these babies’ trajectory of postnatal growth and their specific nutritional requirements with a view to preventing, or at least limiting, long-term complications. In this setting, untargeted metabolomics—a relatively new field of ‘-omics’ research—can be a good way to investigate the metabolic perturbations typically associated with IUGR. The aim of this narrative review is to provide a general overview of the pathophysiological and clinical aspects of IUGR, focusing on evidence emerging from metabolomic studies. Though still only preliminary, the reports emerging so far suggest an “early” pattern of glucose intolerance, insulin resistance, catabolite accumulation, and altered amino acid metabolism in IUGR neonates. Further, larger studies are needed to confirm these results and judge their applicability to clinical practice.

scholarly journals Isolated Hypomethylation of IGF2 Associated with Severe Hypoglycemia Responsive to Growth Hormone Treatment

Diagnostics ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 749
Author(s):  
Sarah C. Grünert ◽  
Uta Matysiak ◽  
Franka Hodde ◽  
Gunda Ruzaike ◽  
Ekkehart Lausch ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Intrauterine Growth Restriction ◽  
Severe Hypoglycemia ◽  
Hormone Treatment ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Poor Growth ◽  
Feeding Difficulties ◽  
Intrauterine Growth ◽  
Pathogenic Variants

Hypomethylation of H19 and IGF2 can cause Silver–Russell syndrome (SRS), a clinically and genetically heterogeneous condition characterized by intrauterine growth restriction, poor postnatal growth, relative macrocephaly, craniofacial abnormalities, body asymmetry, hypoglycemia and feeding difficulties. Isolated hypomethylation of IGF2 has been reported in single cases of SRS as well. Here, we report on a 19-month-old patient who presented with two episodes of hypoglycemic seizures. No intrauterine growth restriction was observed, the patient did not present with SRS-typical facial features, and postnatal growth in the first months of life was along the lower normal percentiles. Exome sequencing did not reveal any likely pathogenic variants explaining the phenotype; however, hypomethylation studies revealed isolated hypomethylation of IGF2, while the methylation of H19 appeared normal. Hypoglycemia responded well to growth hormone therapy, and the boy showed good catch-up growth. Our case demonstrates that SRS and isolated IGF2 hypomethylation should be considered early in the diagnosis of recurrent hypoglycemia in childhood, especially in combination with small gestational age and poor growth.

The placental mTOR-pathway: correlation with early growth trajectories following intrauterine growth restriction?

2015 ◽  
Vol 6 (4) ◽  
pp. 317-326 ◽  
Author(s):  
F. B. Fahlbusch ◽  
A. Hartner ◽  
C. Menendez-Castro ◽  
S. C. Nögel ◽  
I. Marek ◽  
...  
Keyword(s):  
Protein Expression ◽  
Intrauterine Growth Restriction ◽  
Mammalian Target Of Rapamycin ◽  
Adult Life ◽  
Postnatal Growth ◽  
Mtor Pathway ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Catch Up ◽  
Signaling Components

Idiopathic intrauterine growth restriction (IUGR) is a result of impaired placental nutrient supply. Newborns with IUGR exhibiting postnatal catch-up growth are of higher risk for cardiovascular and metabolic co-morbidities in adult life. Mammalian target of rapamycin (mTOR) was recently shown to function as a placental nutrient sensor. Thus, we determined possible correlations of members of the placental mTOR signaling cascade with auxologic parameters of postnatal growth. The protein expression and activity of mTOR-pathway signaling components, Akt, AMP-activated protein kinase α, mTOR, p70S6kinase1 and insulin receptor substrate-1 were analysed via western blotting in IUGR v. matched appropriate-for-gestational age (AGA) placentas. Moreover, mTOR was immunohistochemically stained in placental sections. Data from western blot analyses were correlated with retrospective auxological follow-up data at 1 year of age. We found significant catch-up growth in the 1st year of life in the IUGR group. MTOR and its activated form are immunohistochemically detected in multiple placental compartments. We identified correlations of placental mTOR-pathway signaling components to auxological data at birth and at 1 year of life in IUGR. Analysis of the protein expression and phosphorylation level of mTOR-pathway components in IUGR and AGA placentas postpartum, however, did not reveal pathognomonic changes. Our findings suggest that the level of activated mTOR correlates with early catch-up growth following IUGR. However, the complexity of signals converging at the mTOR nexus and its cellular distribution pattern seem to limit its potential as biomarker in this setting.

The Methylation Status in the Chromosome 11p15.5 Region and Metabolic Disorders in Children with Syndromic and Nonsyndromic Intrauterine Growth Restriction

2021 ◽  
pp. 1-9
Author(s):  
Emre Özer ◽  
Filiz Geyik ◽  
Zeynep Alp Ünkar ◽  
Oya Ercan ◽  
Beyhan Tüysüz
Keyword(s):  
Intrauterine Growth Restriction ◽  
Methylation Status ◽  
Uniparental Disomy ◽  
Postnatal Growth ◽  
Clinical Findings ◽  
Growth Restriction ◽  
Metabolic Complications ◽  
Maternal Uniparental Disomy ◽  
Intrauterine Growth ◽  
Chromosome 11P15.5

Loss of methylation (LoM) of the imprinting control region 1 (ICR1) in the chromosome 11p15.5 domain is detected in patients with Silver-Russell syndrome (SRS), characterized by asymmetric pre- and postnatal growth restriction, and typical craniofacial features. The patients with intrauterine growth restriction (IUGR) possess a high risk for adult metabolic problems. This study is aimed to investigate the methylation levels of the chromosome 11p15.5 region and metabolic problems in children with syndromic and nonsyndromic IUGR. Methylation analysis was performed for chromosome 11p15.5 in 49 patients (33 with suspected SRS and 16 nonsyndromic IUGR) with Netchine-Harbison clinical scoring (NHCS); uniparental disomy for chromosomes 6, 7, 14, and 20 was evaluated for those who were negative. LoM of ICR1 was detected in 14 of 33 suspected SRS patients with 3 or more criteria of NHCS, 5 had borderline LoM. Maternal uniparental disomy of the chromosomes 7 and 14 was found in 2 patients. The overall detection rate of SRS was 45.5%. While clinical findings were similar in patients with LoM and borderline LoM of ICR1, typical craniofacial findings were significantly less in the patients with normal methylation. Methylation patterns were not found to be impaired in the nonsyndromic IUGR group. Metabolic complications were evaluated in a total of 63 patients including 33 SRS-suspicious, 16 nonsyndromic IUGR, and 14 patients with 3M or SHORT syndrome. Increased rates of hypercalciuria, insulin resistance, and dyslipidemia were detected in patients with both syndromic and nonsyndromic IUGR. We would like to emphasize that detecting typical facial findings is effective in the diagnosis of SRS and paying attention to metabolic problems in the follow-up of patients with IUGR is recommended.

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