Facts and hypotheses about the programming of neuroplastic deficits by prenatal malnutrition

Barra, Rafael; Morgan, Carlos; Sáez-Briones, Patricio; Reyes‐Parada, Miguel; Burgos, Héctor; Morales, Bernardo; Hernández, Alejandro

doi:10.1093/nutrit/nuy047

Cited by 12 publications

(10 citation statements)

References 190 publications

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“…Two meta-analyses described the effects of maternal malnutrition on the learning, memory, and behaviour of the schoolchildren who were small for their gestational age. These children exhibited cognitive impairments, lower verbal and performance IQ, and more behavioural disorders than the children in the control group (271,284,285).…”

Section: Effects Of Maternal Undernutrition On Brain and Behavioural ...mentioning

confidence: 80%

“…Global caloric and/or protein restriction during gestation is correlated with deficits in exploration, social behaviour, emotionality, avoidance conditioning, learning, and memory in adult life (270)(271)(272)(273)(274)(275). Batista et al observed that maternal protein malnutrition caused autism spectrum disorder in rat offspring (276).…”

Section: Effects Of Maternal Undernutrition On Brain and Behavioural ...mentioning

confidence: 99%

“…BDNF and insulin-like growth factor (IGF) (252,275). Additionally, the offspring of malnourished rats exhibited changes in their central neurochemical profiles, such as altered NMDA transmission and receptor composition, a decrease in the synaptic NO in the hippocampus (252,281), enhanced GABA-ergic inputs to the hippocampus, and unfavourable changes in the noradrenergic, serotonergic, and dopaminergic transmission (252,271,282,283). Consequently, nutrition-induced deficits in the synaptic transmission impaired memory formation and the LTP (long-term potentiation) (252).…”

Section: Effects Of Maternal Undernutrition On Brain and Behavioural ...mentioning

confidence: 99%

“…Consequently, nutrition-induced deficits in the synaptic transmission impaired memory formation and the LTP (long-term potentiation) (252). Barra et al suggested that prenatal malnutrition-induced brain disturbances depend on two mechanisms: i) the direct effect of foetal programming on the brain, including negative epigenetic changes in foetal progenitor cells and developing neurons, which will form the cerebral cortex, hippocampus, and other brain regions involved in neuroplasticity, and ii) the indirect effect on the brain mediated by the postnatal development of obesity/ metabolic syndrome (271).…”

Section: Effects Of Maternal Undernutrition On Brain and Behavioural ...mentioning

confidence: 99%

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Animal Foetal Models of Obesity and Diabetes – From Laboratory to Clinical Settings

et al. 2022

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The prenatal period, during which a fully formed newborn capable of surviving outside its mother’s body is built from a single cell, is critical for human development. It is also the time when the foetus is particularly vulnerable to environmental factors, which may modulate the course of its development. Both epidemiological and animal studies have shown that foetal programming of physiological systems may alter the growth and function of organs and lead to pathology in adulthood. Nutrition is a particularly important environmental factor for the pregnant mother as it affects the condition of offspring. Numerous studies have shown that an unbalanced maternal metabolic status (under- or overnutrition) may cause long-lasting physiological and behavioural alterations, resulting in metabolic disorders, such as obesity and type 2 diabetes (T2DM). Various diets are used in laboratory settings in order to induce maternal obesity and metabolic disorders, and to alter the offspring development. The most popular models are: high-fat, high-sugar, high-fat-high-sugar, and cafeteria diets. Maternal undernutrition models are also used, which results in metabolic problems in offspring. Similarly to animal data, human studies have shown the influence of mothers’ diets on the development of children. There is a strong link between the maternal diet and the birth weight, metabolic state, changes in the cardiovascular and central nervous system of the offspring. The mechanisms linking impaired foetal development and adult diseases remain under discussion. Epigenetic mechanisms are believed to play a major role in prenatal programming. Additionally, sexually dimorphic effects on offspring are observed. Therefore, further research on both sexes is necessary.

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Section: Effects Of Maternal Undernutrition On Brain and Behavioural ...mentioning

confidence: 80%

Section: Effects Of Maternal Undernutrition On Brain and Behavioural ...mentioning

confidence: 99%

Section: Effects Of Maternal Undernutrition On Brain and Behavioural ...mentioning

confidence: 99%

Section: Effects Of Maternal Undernutrition On Brain and Behavioural ...mentioning

confidence: 99%

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Animal Foetal Models of Obesity and Diabetes – From Laboratory to Clinical Settings

et al. 2022

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“…Based on current evidence, DNA methylation is likely a possible mechanism underlying the effects of fetal malnutrition on impaired organ development. 30,31 This study therefore performed the genome-wide 850K DNA methylation scans to identify CpG sites related to fetal malnutrition. A total of 961 CpG sites were identified, and some of these CpG sites have been reported in previous famine studies using Illumina 450k arrays.…”

Section: Discussionmentioning

confidence: 99%

Fetal malnutrition is associated with impairment of endogenous melatonin synthesis in pineal via hypermethylation of promoters of protein kinase C alpha and cAMP response element‐binding

Han

Jiang

et al. 2021

Journal of Pineal Research

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This study investigated whether and how fetal malnutrition would influence endogenous melatonin synthesis, and whether such effect of fetal malnutrition would transmit to the next generation. We enrolled 2466 participants and 1313 of their offspring. The urine 6-hydroxymelatonin sulfate and serum melatonin rhythm were measured. Methylation microarray detection and bioinformatics analysis were performed to identify hub methylated sites. Additionally, rat experiment was performed to elucidate mechanisms. The participants with fetal malnutrition had lower 6-hydroxymelatonin sulfate (16.59 ± 10.12 μg/24 hours vs 24.29 ± 11.99 μg/24 hours, P < .001) and arear under curve of melatonin rhythm (67.11 ± 8.16 pg/mL vs 77.11 ± 8.04 pg/mL, P < .001). We identified 961 differentially methylated sites, in which the hub methylated sites were locating on protein kinase C alpha (PRKCA) and cAMP response element-binding protein (CREB1) promoters, mediating the association of fetal malnutrition with impaired melatonin secretion. However, such effects were not observed in the offspring (all P > .05). Impaired histomorphology of pineal, decreased melatonin in serum, pineal, and pinealocyte were also found in the in vivo and in vitro

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Biological basis of neurodevelopmental disabilities

Kielty,

Risen,

Melendez-Zaidi

2025

Capute and Accardo' S Neurodevelopmental Disabilities in Infancy and Childhood

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Facts and hypotheses about the programming of neuroplastic deficits by prenatal malnutrition

Cited by 12 publications

References 190 publications

Animal Foetal Models of Obesity and Diabetes – From Laboratory to Clinical Settings

Animal Foetal Models of Obesity and Diabetes – From Laboratory to Clinical Settings

Fetal malnutrition is associated with impairment of endogenous melatonin synthesis in pineal via hypermethylation of promoters of protein kinase C alpha and cAMP response element‐binding

Biological basis of neurodevelopmental disabilities

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