scholarly journals Fetal growth restriction shortens cardiac telomere length, but this is attenuated by exercise in early life

2018 ◽  
Vol 50 (11) ◽  
pp. 956-963
Author(s):  
S. A. Booth ◽  
G. D. Wadley ◽  
F. Z. Marques ◽  
M. E. Wlodek ◽  
F. J. Charchar
Keyword(s):  
Telomere Length ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Early Life ◽  
Protein Structures ◽  
Later Life ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Male Rats ◽  
Early Exercise

Background and aims: Fetal and postnatal growth restriction cause a predisposition to cardiovascular disease (CVD) in adulthood. Telomeres are repetitive DNA-protein structures that protect chromosome ends, and the loss of these repeats (a reduction in telomere length) is associated with CVD. As exercise preserves telomere length and cardiovascular health, the aim of this study was to determine the effects of growth restriction and exercise training on cardiac telomere length and telomeric genes. Methods and results: Pregnant Wistar Kyoto rats underwent bilateral uterine vessel ligation to induce uteroplacental insufficiency and fetal growth restriction (“Restricted”). Sham-operated rats had either intact litters (“Control”) or their litters reduced to five pups with slowed postnatal growth (“Reduced”). Control, Restricted, and Reduced male rats were assigned to Sedentary, Early exercise (5–9 wk of age), or Late exercise (20–24 wk of age) groups. Hearts were excised at 24 wk of age for telomere length and gene expression measurements by quantitative PCR. Growth restriction shortened cardiac telomere length ( P < 0.001), but this was rescued by early exercise ( P < 0.001). Early and Late exercise increased cardiac weight index ( P < 0.001), but neither this nor telomere length was associated with expression of the telomeric genes Tert, Terc, Trf2, Pnuts, or Sirt1. Discussion and conclusions: Growth restriction shortens cardiac telomere length, reflecting the cardiac pathologies associated with low birth weight. Exercise in early life may offer long-term protective effects on cardiac telomere length, which could help prevent CVD in later life.

scholarly journals The transition from fetal growth restriction to accelerated postnatal growth: a potential role for insulin signalling in skeletal muscle

2009 ◽  
Vol 587 (17) ◽  
pp. 4199-4211 ◽  
Author(s):  
B. S. Muhlhausler ◽  
J. A. Duffield ◽  
S. E. Ozanne ◽  
C. Pilgrim ◽  
N. Turner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Potential Role ◽  
Insulin Signalling ◽  
Postnatal Growth ◽  
Growth Restriction

scholarly journals Placenta-specific Slc38a2/SNAT2 knockdown causes fetal growth restriction in mice.

2021 ◽  
Author(s):  
Owen Vaughan ◽  
Katarzyna Maksym ◽  
Elena Silva ◽  
Kenneth Barentsen ◽  
Russel V Anthony ◽  
...  
Keyword(s):  
Amino Acid ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Late Onset ◽  
Specific Treatment ◽  
Later Life ◽  
Growth Restriction ◽  
Amino Acid Transport System ◽  
Mortality And Morbidity ◽  
Appropriate For Gestational Age

Fetal growth restriction (FGR) is a complication of pregnancy that reduces birth weight, markedly increases infant mortality and morbidity and is associated with later-life cardiometabolic disease.  No specific treatment is available for FGR. Placentas of human FGR infants have low abundance of sodium-coupled neutral amino acid transporter 2 (Slc38a2/SNAT2), which supplies the fetus with amino acids required for growth. We determined the mechanistic role of placental Slc38a2/SNAT2 deficiency in the development of restricted fetal growth, hypothesizing that placenta-specific Slc38a2 knockdown causes fetal growth restriction in mice. Using lentiviral transduction of blastocysts with a small hairpin RNA, we achieved 59% knockdown of placental Slc38a2, without altering fetal Slc38a2 expression. Placenta-specific Slc38a2 knockdown reduced near-term fetal and placental weight, fetal viability, trophoblast plasma membrane SNAT2 protein abundance, and both absolute and weight-specific placental uptake of the amino acid transport System A tracer, 14C-methylaminoisobutyric acid. We also measured human placental SLC38A2 gene expression in a well-defined term clinical cohort and found that SLC38A2 expression was decreased in late-onset, but not early-onset FGR, compared to appropriate for gestational age control placentas. The results demonstrate that low placental Slc38a2/SNAT2 causes fetal growth restriction and could be a target for clinical therapies for late-onset FGR.

scholarly journals 252: Placental telomere length in preterm fetal growth restriction due to placental insufficiency

2017 ◽  
Vol 216 (1) ◽  
pp. S156-S157
Author(s):  
Kiesha N. Benn ◽  
Christine Abreu ◽  
Jeanne D. Rolle ◽  
Ye Sun ◽  
Chia-ling Kuo ◽  
...  
Keyword(s):  
Telomere Length ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Placental Insufficiency ◽  
Growth Restriction

scholarly journals Diagnosis and Management of Fetal Growth Restriction

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Jacqueline E. A. K. Bamfo ◽  
Anthony O. Odibo
Keyword(s):  
Metabolic Syndrome ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Clinical Management ◽  
Later Life ◽  
Growth Restriction ◽  
Surveillance Program ◽  
Mortality And Morbidity ◽  
Diagnosis And Management ◽  
Biophysical Profile

Fetal growth restriction (FGR) remains a leading contributor to perinatal mortality and morbidity and metabolic syndrome in later life. Recent advances in ultrasound and Doppler have elucidated several mechanisms in the evolution of the disease. However, consistent classification and characterization regarding the severity of FGR is lacking. There is no cure, and management is reliant on a structured antenatal surveillance program with timely intervention. Hitherto, the time to deliver is an enigma. In this paper, the challenges in the diagnosis and management of FGR are discussed. The biophysical profile, Doppler, biochemical and molecular technologies that may refine management are reviewed. Finally, a model pathway for the clinical management of pregnancies complicated by FGR is presented.

Cognitive outcome in childhood of birth weight discordant monochorionic twins: the long-term effects of fetal growth restriction

2018 ◽  
Vol 103 (6) ◽  
pp. F512-F516 ◽  
Author(s):  
Ravi Shankar Swamy ◽  
Helen McConachie ◽  
Jane Ng ◽  
Judith Rankin ◽  
Murthy Korada ◽  
...  
Keyword(s):  
Birth Weight ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Later Life ◽  
Mean Difference ◽  
Growth Restriction ◽  
Cognitive Outcome ◽  
Monochorionic Twins ◽  
Monochorionic Twin ◽  
Twin Model

AimIntrauterine growth restriction (IUGR) is associated with poorer outcomes in later life. We used a monochorionic twin model with IUGR in one twin to determine its impact on growth and neurocognitive outcomes.MethodsMonochorionic twins with ≥20% birth weight discordance born in the north of England were eligible. Cognitive function was assessed using the British Ability Scales. The Strength and Difficulties Questionnaire was used to identify behavioural problems. Auxological measurements were collected. Generalised estimating equations were used to determine the effects of birth weight on cognition.ResultsFifty-one monochorionic twin pairs were assessed at a mean age of 6.3 years. Mean birth weight difference was 664 g at a mean gestation of 34.7 weeks. The lighter twin had a General Conceptual Ability (GCA) score that was three points lower (TwinL −105.4 vs TwinH −108.4, 95% CI −0.9 to −5.0), and there was a significant positive association (B 0.59) of within-pair birth weight differences and GCA scores. Mathematics and memory skills showed the largest differences. The lighter twin at school age was shorter (mean difference 2.1 cm±0.7) and lighter (mean difference 1.9 kg±0.6). Equal numbers of lighter and heavier twins were reported to have behavioural issues.ConclusionsIn a monochorionic twin cohort, fetal growth restriction results in lower neurocognitive scores in early childhood, and there remain significant differences in size. Longer term follow-up will be required to determine whether growth or cognitive differences persist in later child or adulthood, and whether there are any associated longer term metabolic sequelae.

FETAL GROWTH RESTRICTION WITH EARLY AND LATE MANIFESTATION, PROGNOSTIC MARKERS

2020 ◽  
pp. 27-30
Author(s):  
Yakubova D.I.
Keyword(s):  
Risk Factors ◽  
Pregnant Women ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Prenatal Screening ◽  
Prognostic Markers ◽  
Growth Restriction ◽  
Late Manifestation ◽  
Late Form ◽  
Early Manifestation

Objective of the study: Comprehensive assessment of risk factors, the implementation of which leads to FGR with early and late manifestation. To evaluate the results of the first prenatal screening: PAPP-A, B-hCG, made at 11-13 weeks. Materials and Methods: A retrospective study included 110 pregnant women. There were 48 pregnant women with early manifestation of fetal growth restriction, 62 pregnant women with late manifestation among them. Results of the study: The risk factors for the formation of the FGR are established. Statistically significant differences in the indicators between groups were not established in the analyses of structures of extragenital pathology. According to I prenatal screening, there were no statistical differences in levels (PAPP-A, b-hCG) in the early and late form of FGR.

Sign in / Sign up

Export Citation Format

Share Document