ArticleFrontiers in endocrinology2019
Why and How Imprinted Genes Drive Fetal Programming.
Article in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- A rapid review of genetic association studies of parent-of-origin effects and fetal growth.Molecular and cellular pediatrics · 2026Review
- DNA methylation of theiScience · 2026Article
- Environmental exposures and epigenetic alterations in common chronic diseases: insights and challenges.Environmental epigenetics · 2026Review
- Reversible Histone Acetylation During Preimplantation Embryo Development in Mammals.Results and problems in cell differentiation · 2025Review
- Sex dimorphic associations of Prader-Willi imprinted gene expressions in umbilical cord with prenatal and postnatal growth in healthy infants.World journal of pediatrics : WJP · 2025Article
- Association between maternal perinatal stress and depression and infant DNA methylation in the first year of life.Translational psychiatry · 2024Article
- Comprehensive Analysis of Placental DNA Methylation Changes and Fetal Birth Weight in Pigs.International journal of molecular sciences · 2024Article
- Association between Maternal Perinatal Stress and Depression on Infant DNA Methylation in the First Year of Life.Research square · 2024Article
- Iconic logic: the visual art of drawing the right conclusion.Frontiers in psychology · 2024Review
- Mendelian randomization shows causal effects of birth weight and childhood body mass index on the risk of frailty.Frontiers in public health · 2024Article
- The geometry of evolutionary conflict.Proceedings. Biological sciences · 2023Article
- Prenatal paternal anxiety symptoms predict child DHEA levels and internalizing symptoms during adrenarche.Frontiers in behavioral neuroscience · 2023Article
- Article
- The Foetal Origins of Allergy and Potential Nutritional Interventions to Prevent Disease.Nutrients · 2022Review
- Iconic Mathematics: Math Designed to Suit the Mind.Frontiers in psychology · 2022Review
- Alteration of Genomic Imprinting after Assisted Reproductive Technologies and Long-Term Health.Life (Basel, Switzerland) · 2021Review
- The role of CTCF in the organization of the centromeric 11p15 imprinted domain interactome.Nucleic acids research · 2021Article
- Pregnancies in Diabetes and Obesity: The Capacity-Load Model of Placental Adaptation.Diabetes · 2021Review
- Mental Health, Mitochondria, and the Battle of the Sexes.Biomedicines · 2021Review
- Diabetic Uterine Environment Leads to Disorders in Metabolism of Offspring.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imprinted genes mediate fetal and childhood growth and development, and early growth patterns drive fetal programming effects. However, predictions and evidence from the kinship theory of imprinting have yet to be directly integrated with data on fetal programming and risks of metabolic disease. I first define paternal-gene and maternal-gene optima with regard to early human growth and development. Next, I review salient evidence with regard to imprinted gene effects on birth weight, body composition, trajectories of feeding and growth, and timing of developmental stages, to evaluate why and how imprinted gene expression influences risks of metabolic disease in later life. I find that metabolic disease risks derive primarily from maternal gene biases that lead to reduced placental efficacy, low birth weight, low relative muscle mass, high relative white fat, increased abdominal adiposity, reduced pancreatic β-cell mass that promotes insulin resistance, reduced appetite and infant sucking efficacy, catch-up fat deposition from family foods after weaning, and early puberty. Paternal gene biases, by contrast, may contribute to metabolic disease via lower rates of brown fat thermiogenesis, and through favoring more rapid postnatal catch-up growth after intrauterine growth restriction from environmental causes. These disease risks can be alleviated through dietary and pharmacological alterations that selectively target imprinted gene expression and relevant metabolic pathways. The kinship theory of imprinting, and mother-offspring conflict more generally, provide a clear predictive framework for guiding future research on fetal programming and metabolic disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.