Programming the brain: Common outcomes and gaps in knowledge from animal studies of IUGR

Hunter, Damien S.; Hazel, Susan J.; Kind, Karen L.; Owens, Julie A.; Pitcher, Julia B.; Gatford, Kathryn L.

doi:10.1016/j.physbeh.2016.06.005

Cited by 37 publications

(41 citation statements)

References 213 publications

(285 reference statements)

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“…As such, the translatability of studies performed in altricial species (mice and rats) should be approached with caution as many key stages of development that occur before birth in humans occur after birth in these species (Dobbing & Sands, ; Hunter et al . ). Thirdly, fetal number should not be excessive.…”

Section: Introductionmentioning

confidence: 97%

Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic

Morrison

Botting

Darby

et al. 2018

The Journal of Physiology

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109

108

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Over 30 years ago Professor David Barker first proposed the theory that events in early life could explain an individual's risk of non-communicable disease in later life: the developmental origins of health and disease (DOHaD) hypothesis. During the 1990s the validity of the DOHaD hypothesis was extensively tested in a number of human populations and the mechanisms underpinning it characterised in a range of experimental animal models. Over the past decade, researchers have sought to use this mechanistic understanding of DOHaD to develop therapeutic interventions during pregnancy and early life to improve adult health. A variety of animal models have been used to develop and evaluate interventions, each with strengths and limitations. It is becoming apparent that effective translational research requires that the animal paradigm selected mirrors the tempo of human fetal growth and development as closely as possible so that the effect of a perinatal insult and/or therapeutic intervention can be fully assessed. The guinea pig is one such animal model that over the past two decades has demonstrated itself to be a very useful platform for these important reproductive studies. This review highlights similarities in the in utero development between humans and guinea pigs, the strengths and limitations of the guinea pig as an experimental model of DOHaD and the guinea pig's potential to enhance clinical therapeutic innovation to improve human health.

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Section: Introductionmentioning

confidence: 97%

Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic

Morrison

Botting

Darby

et al. 2018

The Journal of Physiology

Self Cite

109

108

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“…ASD prevalence in the United States has increased dramatically since 1996 and now, 1 in 68 children are diagnosed with ASD [Krakowiak et al, 2012;Van Naarden Braun et al, 2015]. The precise cause is a proxy for intrauterine growth restriction [Hunter et al, 2016] and studies have reported that SGA children are at increased risk of ASD [Lampi et al, 2012;Larsson et al, 2005;Moore et al, 2012]; however, the results are inconsistent [Glasson et al, 2004;Larsson et al, 2005;Schendel & Bhasin, 2008]. Many children that are small at birth tend to have rapid catch-up growth during early postnatal period [Castanys-Munoz et al, 2017;Ong, 2007].…”

Section: Introductionmentioning

confidence: 99%

Fetal and Infancy Growth Pattern, Cord and Early Childhood Plasma Leptin, and Development of Autism Spectrum Disorder in the Boston Birth Cohort

et al. 2018

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Leptin is a pro-inflammatory cytokine that plays an important role in energy homeostasis. Emerging evidence suggests that leptin levels are altered in children with autism spectrum disorder (ASD); however this has not been studied prospectively. Rapid growth during infancy and early childhood has been implicated in ASD, but the evidence is inconsistent. Since leptin is involved in growth and is a potential risk factor for ASD, we explored the associations between 1) cord, early childhood leptin and ASD; and 2) birth weight for gestational age, early childhood weight gain and ASD. We also assessed the mediating role of leptin in the relationship between weight gain during infancy and ASD. This study was conducted in a sample of 822 subjects from the Boston Birth Cohort. ASD was defined from diagnostic codes in electronic medical records. Extremely rapid weight gain during infancy was associated with a greater ASD risk and this persisted after adjusting for potential confounders (aOR: 3.11; 95% CI: 1.37, 7.07). Similarly, children that had higher plasma leptin levels, prior to ASD diagnosis, had an increased ASD risk in both unadjusted and adjusted models (aOR: 7.87; 95% CI: 2.06, 30.04). Further, early childhood leptin indirectly mediated the relationship between rapid weight gain and ASD. No associations were found between birth weight for gestational age, cord leptin and risk of ASD. Our findings provide a basis to further explore whether the combination of early life growth pattern and a biomarker such as leptin can predict ASD earlier.

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“…The former include maternal diet, maternal smoking, alcoholism, hypertension, malnutrition, trace elements, stress, diabetes, substance use, and exposure to environmental toxicants (Lyall et al, ) (Al‐Gubory, ). The latter include fetal hypoxia/asphyxia, placental insufficiency, prematurity, low birth weight, drugs administered to the mother or to the baby in the perinatal period and, in general, all factors causing intrauterine growth restriction (IUGR) (Hunter et al, ). Recently, in an experimental model of asphyxia‐reoxygenation, the use of 100% oxygen was associated with high levels of neuronal cell death in the brain cortex, indicating oxygen overexposure as a possible cause of neural loss in the perinatal period (Faa et al, ).…”

Section: Introductionmentioning

confidence: 99%

Fetal programming of neuropsychiatric disorders

Faa

Manchia

Pintus

et al. 2016

Birth Defects Research Pt C

131

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Starting from the Developmental Origins of Health and Disease (DOHaD) hypotheses proposed by David Barker, namely fetal programming, in the past years, there is a growing evidence of the major role played by epigenetic factors during the intrauterine life and the perinatal period. Furthermore, it has been assessed that these factors can affect the health status in infancy and even in adulthood. In this review, we focus our attention on the fetal programming of the brain, analyzing the most recent literature concerning the epigenetic factors that can influence the development of neuropsychiatric disorders such as bipolar disorders, major depressive disorders, and schizophrenia. The perinatal epigenetic factors have been divided in two main groups: maternal factors and fetal factors. The maternal factors include diet, smoking, alcoholism, hypertension, malnutrition, trace elements, stress, diabetes, substance abuse, and exposure to environmental toxicants, while the fetal factors include hypoxia/asphyxia, placental insufficiency, prematurity, low birth weight, drugs administered to the mother or to the baby, and all factors causing intrauterine growth restriction. A better comprehension of the possible mechanisms underlying the pathogenesis of these diseases may help researchers and clinicians develop new diagnostic tools and treatments to offer these patients a tailored medical treatment strategy to improve their quality of life. Birth Defects Research (Part C) 108:207-223, 2016. © 2016 Wiley Periodicals, Inc.

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Programming the brain: Common outcomes and gaps in knowledge from animal studies of IUGR

Cited by 37 publications

References 213 publications

Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic

Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic

Fetal and Infancy Growth Pattern, Cord and Early Childhood Plasma Leptin, and Development of Autism Spectrum Disorder in the Boston Birth Cohort

Fetal programming of neuropsychiatric disorders

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