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BMC Pediatrics Aug 2022Preeclampsia is a hypertensive disorder of pregnancy with serious health implications for mother and their offspring. The uteroplacental vascular insufficiency caused by... (Review)
Review
Preeclampsia is a hypertensive disorder of pregnancy with serious health implications for mother and their offspring. The uteroplacental vascular insufficiency caused by preeclampsia is associated with epigenetic and pathological changes in the mother and fetus. However, the impact of preeclampsia in infancy (birth to 2 years), a time of rapid development influenced by pre- and postnatal factors that can predict future health outcomes, remains inconclusive. This narrative review of 23 epidemiological and basic science studies assessed the measurement and impact of preeclampsia exposure on infant growth and psychomotor developmental outcomes from birth to 2 years. Studies assessing infant growth report that preeclampsia-exposed infants have lower weight, length and BMI at 2 years than their normotensive controls, or that they instead experience accelerated weight gain to catch up in growth by 2 years, which may have long-term implications for their cardiometabolic health. In contrast, clear discrepancies remain as to whether preeclampsia exposure impairs infant motor and cognitive development, or instead has no impact. It is additionally unknown whether any impacts of preeclampsia are independent of confounders including shared genetic factors that predispose to both preeclampsia and childhood morbidity, perinatal factors including small for gestational age or preterm birth and their sequelae, and postnatal environmental factors such childhood nutrition. Further research is required to account for these variables in larger cohorts born at term, to help elucidate the independent pathophysiological impact of this clinically heterogenous and dangerous disease.
Topics: Child; Female; Fetal Growth Retardation; Humans; Infant; Infant, Newborn; Infant, Small for Gestational Age; Pre-Eclampsia; Pregnancy; Premature Birth; Weight Gain
PubMed: 36042465
DOI: 10.1186/s12887-022-03542-5 -
JAMA Network Open Dec 2021Preterm birth and low birth weight are associated with brain developmental and neurocognitive outcomes in childhood; however, not much is known about the specific...
IMPORTANCE
Preterm birth and low birth weight are associated with brain developmental and neurocognitive outcomes in childhood; however, not much is known about the specific critical periods in fetal life and infancy for these outcomes.
OBJECTIVE
To examine the associations of fetal and infant growth patterns with brain morphology in children at school age.
DESIGN, SETTING, AND PARTICIPANTS
This population-based, prospective cohort study was conducted from February 1 to April 16, 2021, as a part of the Generation R Study in Rotterdam, the Netherlands. The study included 3098 singleton children born between April 1, 2002, and January 31, 2006.
EXPOSURES
Fetal weight was estimated in the second and third trimesters of pregnancy by ultrasonography. Infant weight was measured at birth and at 6, 12, and 24 months. Fetal and infant weight acceleration or deceleration were defined as a change in SD scores greater than 0.67 between time points. Infant measurements also included peak weight velocity, and age and body mass index reached at adiposity peak.
MAIN OUTCOMES AND MEASURES
Brain structure, including global and regional brain volumes, was quantified by magnetic resonance imaging at age 10 years.
RESULTS
The study evaluated 3098 children (mean [SD] age at follow-up, 10.1 [0.6] years; 1557 girls [50.3%]; and 1753 Dutch [57.8%]). One SD score-higher weight gain until the second and third trimesters, birth, and 6, 12, and 24 months was associated with larger total brain volume independently of growth during any other age windows (second trimester: 5.7 cm3; 95% CI, 1.2-10.2 cm3; third trimester: 15.3 cm3; 95% CI, 11.0-19.6 cm3; birth: 20.8 cm3; 95% CI, 16.4-25.1 cm3; 6 months: 15.6 cm3; 95% CI, 11.2-19.9 cm3; 12 months: 11.3 cm3; 95% CI, 7.0-15.6 cm3; and 24 months: 11.1 cm3; 95% CI, 6.8-15.4 cm3). Compared with children with normal fetal and infant growth, those with fetal and infant growth deceleration had the smallest total brain volume (-32.5 cm3; 95% CI, -53.2 to -11.9 cm3). Children with fetal weight deceleration followed by infant catch-up growth had similar brain volumes as children with normal growth. Higher peak weight velocity and body mass index reached at adiposity peak were associated with larger brain volumes. Similar results were observed for cerebral and cerebellar gray and white matter volumes.
CONCLUSIONS AND RELEVANCE
This cohort study's findings suggest that both fetal and infant weight growth might be critical for cerebral and cerebellar brain volumes during childhood. Whether these associations link to neurocognitive outcomes should be further studied.
Topics: Adult; Body Mass Index; Brain; Child; Child Development; Child, Preschool; Cohort Studies; Female; Fetal Development; Humans; Infant; Infant, Newborn; Male; Netherlands; Prospective Studies; Weight Gain
PubMed: 34882181
DOI: 10.1001/jamanetworkopen.2021.38214 -
The American Journal of Clinical... Oct 2022
Topics: Acceleration; Child; Female; Glucose; Humans; Infant; Infant Formula; Lactose; Obesity; Weight Gain; Zea mays
PubMed: 35998081
DOI: 10.1093/ajcn/nqac191 -
Journal of Developmental Origins of... Apr 2021Sleep-disordered breathing (SDB) worsens over pregnancy, and obstructive sleep apnea is associated with serious maternal complications. Intrauterine exposures that... (Review)
Review
Sleep-disordered breathing (SDB) worsens over pregnancy, and obstructive sleep apnea is associated with serious maternal complications. Intrauterine exposures that provoke insulin resistance (IR), inflammation, or oxidative stress may have long-term offspring health consequences. In obesity, worsening maternal SDB appears to be an exposure that increases the risk for both small- or large-for-gestational-age (SGA, LGA, respectively), suggesting distinct outcomes linked to a common maternal phenotype. The aim of this paper is to systematically review and link data from both mechanistic rodent models and descriptive human studies to characterize the impact of maternal SDB on fetal development. A systematic review of the literature was conducted using PubMed, Embase, and CINAHL (01/2000-09/2019). Data from rodent (9 studies) and human models (48 studies, 5 meta-analyses) were included and reviewed using PRISMA guidelines. Evidence from rodent models suggests that intermittent maternal hypoxia results in mixed changes in birth weight (BW) followed by accelerated postnatal growth, while maternal sleep fragmentation results in normal BW followed by later metabolic derangement. Human studies support that maternal SDB is associated with both SGA and LGA, both of which may predispose offspring to later obesity. Evidence also suggests a link between SDB, inflammation, and oxidative stress that may impact maternal metabolism and/or placental function. SDB is common in pregnancy and affects fetal growth and development. Given that SDB has significant potential to adversely influence the intrauterine metabolic environment, larger, prospective studies in humans are urgently needed to fully elucidate the effects of this exposure on offspring metabolic risk.
Topics: Birth Weight; Female; Gestational Age; Humans; Infant, Newborn; Pediatric Obesity; Pregnancy; Pregnancy Complications; Sleep Apnea Syndromes
PubMed: 32425147
DOI: 10.1017/S2040174420000355 -
Journal of Applied Physiology... Feb 2022Nearly one-third of children in the United States are overweight or obese by their preteens. Tall stature and accelerated bone elongation are characteristic features of...
Nearly one-third of children in the United States are overweight or obese by their preteens. Tall stature and accelerated bone elongation are characteristic features of childhood obesity, which cooccur with conditions such as limb bowing, slipped epiphyses, and fractures. Children with obesity paradoxically have normal circulating IGF-I, the major growth-stimulating hormone. Here, we describe and validate a mouse model of excess dietary fat to examine mechanisms of growth acceleration in obesity. We used in vivo multiphoton imaging and immunostaining to test the hypothesis that high-fat diet increases IGF-I activity and alters growth plate structure before the onset of obesity. We tracked bone and body growth in male and female C57BL/6 mice ( = 114) on high-fat (60% kcal fat) or control (10% kcal fat) diets from weaning (3 wk) to skeletal maturity (12 wk). Tibial and tail elongation rates increased after brief (1-2 wk) high-fat diet exposure without altering serum IGF-I. Femoral bone density and growth plate size were increased, but growth plates were disorganized in not-yet-obese high-fat diet mice. Multiphoton imaging revealed more IGF-I in the vasculature surrounding growth plates of high-fat diet mice and increased uptake when vascular levels peaked. High-fat diet growth plates had more activated IGF-I receptors and fewer inhibitory binding proteins, suggesting increased IGF-I bioavailability in growth plates. These results, which parallel pediatric growth patterns, highlight the fundamental role of diet in the earliest stages of developing obesity-related skeletal complications and validate the utility of the model for future studies aimed at determining mechanisms of diet-enhanced bone lengthening. This paper validates a mouse model of linear growth acceleration in juvenile obesity. We demonstrate that high-fat diet induces rapid increases in bone elongation rate that precede excess weight gain and parallel pediatric growth. By imaging IGF-I delivery to growth plates in vivo, we reveal novel diet-induced changes in IGF-I uptake and activity. These results are important for understanding the sequelae of musculoskeletal complications that accompany advanced bone age and obesity in children.
Topics: Animals; Child; Diet, High-Fat; Female; Growth Plate; Humans; Insulin-Like Growth Factor I; Male; Mice; Mice, Inbred C57BL; Pediatric Obesity; Weight Gain
PubMed: 34989650
DOI: 10.1152/japplphysiol.00431.2021 -
Problemy Endokrinologii Oct 2022The article presents data about short stature due to intrauterine development delay. This type of short stature - separate nosology, unites children born small for...
The article presents data about short stature due to intrauterine development delay. This type of short stature - separate nosology, unites children born small for gestation age. The majority of them in the first years of life have accelerated growth rates, allowing the child to normalize their weight-growth indicators and catch up in the development of peers. In the absence of an accelerated growth rates, children have a high risk of lagging behind in physical development throughout childhood, achieving low final growth and becoming short adults. In addition, the fact of birth with small body sizes is associated with a number of hormonal and metabolic features, a risk of metabolic syndrome in adult years.It is assumed that the absence of postnatal growth acceleration is due to various damages to the GH-IGF1 axis (partial GH deficiency, partial resistance to GH, partial resistance to IGF1). Growth hormone therapy, initiated early in life, is able to normalize growth rates in childhood and ultimately significantly improve or normalize the final growth of short stature children born small for gestational age.
Topics: Infant, Newborn; Child; Adult; Female; Humans; Fetal Growth Retardation; Body Height; Infant, Small for Gestational Age; Human Growth Hormone; Growth Hormone; Dwarfism
PubMed: 36337013
DOI: 10.14341/probl13178 -
Scientific Reports Jun 2023Knowledge of human craniofacial growth (increase in size) and development (change in shape) is important in the clinical treatment of a range of conditions that affects...
Knowledge of human craniofacial growth (increase in size) and development (change in shape) is important in the clinical treatment of a range of conditions that affects it. This study uses an extensive collection of clinical CT scans to investigate craniofacial growth and development over the first 48 months of life, detail how the cranium changes in form (size and shape) in each sex and how these changes are associated with the growth and development of various soft tissues such as the brain, eyes and tongue and the expansion of the nasal cavity. This is achieved through multivariate analyses of cranial form based on 3D landmarks and semi-landmarks and by analyses of linear dimensions, and cranial volumes. The results highlight accelerations and decelerations in cranial form changes throughout early childhood. They show that from 0 to 12 months, the cranium undergoes greater changes in form than from 12 to 48 months. However, in terms of the development of overall cranial shape, there is no significant sexual dimorphism in the age range considered in this study. In consequence a single model of human craniofacial growth and development is presented for future studies to examine the physio-mechanical interactions of the craniofacial growth.
Topics: Humans; Child, Preschool; Skull; Acceleration; Brain; Eye; Growth and Development
PubMed: 37316540
DOI: 10.1038/s41598-023-36646-8 -
ELife Sep 2021In fluctuating environments, switching between different growth strategies, such as those affecting cell size and proliferation, can be advantageous to an organism....
In fluctuating environments, switching between different growth strategies, such as those affecting cell size and proliferation, can be advantageous to an organism. Trade-offs arise, however. Mechanisms that aberrantly increase cell size or proliferation-such as mutations or chemicals that interfere with growth regulatory pathways-can also shorten lifespan. Here we report a natural example of how the interplay between growth and lifespan can be epigenetically controlled. We find that a highly conserved RNA-modifying enzyme, the pseudouridine synthase Pus4/TruB, can act as a prion, endowing yeast with greater proliferation rates at the cost of a shortened lifespan. Cells harboring the prion grow larger and exhibit altered protein synthesis. This epigenetic state, [] (etter n rowth), allows cells to heritably yet reversibly alter their translational program, leading to the differential synthesis of dozens of proteins, including many that regulate proliferation and aging. Our data reveal a new role for prion-based control of an RNA-modifying enzyme in driving heritable epigenetic states that transform cell growth and survival.
Topics: Cell Enlargement; Cell Proliferation; Epigenesis, Genetic; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Fungal; HSP70 Heat-Shock Proteins; Intramolecular Transferases; Longevity; Meiosis; Prion Proteins; Protein Biosynthesis; Saccharomyces cerevisiae; Saccharomyces cerevisiae Proteins; Time Factors
PubMed: 34545808
DOI: 10.7554/eLife.60917 -
The Journal of Maternal-fetal &... Jul 2020The growth of the fetus is a complex process, influenced by genetic and environmental factors. Longitudinal patterns of fetal growth are required to fully understand... (Randomized Controlled Trial)
Randomized Controlled Trial
The growth of the fetus is a complex process, influenced by genetic and environmental factors. Longitudinal patterns of fetal growth are required to fully understand this process, however to date, a paucity of data exists in this area.Objective: To identify fetal growth trajectories in-utero and to assess their association with maternal and child characteristics up to 5 years postnatal. Data from 781 mother-child pairs from the ROLO longitudinal birth cohort study were analyzed. The ROLO study was a randomized control trial of a low glycemic index diet in pregnancy to prevent recurrence of macrosomia. Fetal ultrasound measurements were recorded at 20 and 34 weeks gestation, and birth weight was recorded. Abdominal circumference (AC), weight (fetal weight, or birth weight), a standardized proxy for length (femur length or birth length, individually standardized), and AC:length ratio were examined for trajectory classes using latent class trajectory mixture models. Two-, three-, four-, and five-class models were evaluated for fit, using a linear (first order) trajectory over three time-points. ANOVA and chi-square tests were applied to test associations between trajectory membership and maternal and child characteristics up to age 5. For AC, two fetal growth trajectories were identified, with 29% of participants on a "slow" trajectory and 71% on a "fast" trajectory. Those on a fast trajectory had higher rates of maternal impaired glucose tolerance (28.7 versus 16.5%, p<.001) and higher rates of mean child 5-year body mass index (BMI) centiles (64th versus 58th centile, p<.05) compared to those on the slow trajectory. For estimated fetal weight, four trajectories were identified, with 4% on a "very-slow" trajectory, 63% in a "moderate-slow" trajectory, 30% in a "moderate-fast" trajectory and 3% on a "very-fast" trajectory. Mothers with a fetus on the fastest trajectory had higher antenatal serum glucose levels (p<.05), and were more likely to deliver by cesarean section (59.1 versus 20%, p<.001). At 5 years of age, children on the fastest growth trajectory had the highest mean BMI centile (86th versus 60th centile, p<.05). This study shows that specific fetal growth trajectories may be associated with maternal serum glucose concentrations during pregnancy, mode of delivery and child BMI at 5 years of age. Diet and lifestyle measures that target maternal glucose levels during pregnancy may have lifelong benefits for children's BMI. Identifying those on an accelerated growth trajectory during fetal life provides a unique opportunity for antenatal and infant interventions that may have long-lasting health benefits.
Topics: Birth Weight; Blood Glucose; Body Mass Index; Cesarean Section; Child, Preschool; Female; Fetal Development; Fetal Weight; Humans; Infant, Newborn; Longitudinal Studies; Male; Pregnancy; Pregnancy Complications; Ultrasonography, Prenatal; Waist Circumference
PubMed: 30614328
DOI: 10.1080/14767058.2018.1554041 -
Development (Cambridge, England) Sep 2022Heart regeneration requires multiple cell types to enable cardiomyocyte (CM) proliferation. How these cells interact to create growth niches is unclear. Here, we profile...
Heart regeneration requires multiple cell types to enable cardiomyocyte (CM) proliferation. How these cells interact to create growth niches is unclear. Here, we profile proliferation kinetics of cardiac endothelial cells (CECs) and CMs in the neonatal mouse heart and find that they are spatiotemporally coupled. We show that coupled myovascular expansion during cardiac growth or regeneration is dependent upon VEGF-VEGFR2 signaling, as genetic deletion of Vegfr2 from CECs or inhibition of VEGFA abrogates both CEC and CM proliferation. Repair of cryoinjury displays poor spatial coupling of CEC and CM proliferation. Boosting CEC density after cryoinjury with virus encoding Vegfa enhances regeneration. Using Mendelian randomization, we demonstrate that circulating VEGFA levels are positively linked with human myocardial mass, suggesting that Vegfa can stimulate human cardiac growth. Our work demonstrates the importance of coupled CEC and CM expansion and reveals a myovascular niche that may be therapeutically targeted for heart regeneration.
Topics: Animals; Cell Proliferation; Endothelial Cells; Heart; Humans; Infant, Newborn; Mice; Myocytes, Cardiac; Signal Transduction; Vascular Endothelial Growth Factor A
PubMed: 36134690
DOI: 10.1242/dev.200654