ReviewFrontiers in endocrinology2017
Experimental Models of Maternal Obesity and Neuroendocrine Programming of Metabolic Disorders in Offspring.
Review in Frontiers in endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- Maternal Nutrition and Hypothalamic Programming of Offspring Metabolic Health.The Journal of nutrition · 2026Review
- Spontaneous Pregravid Obesity Reshapes Fetal Immune Ontogeny in a Nonhuman Primate Model.bioRxiv : the preprint server for biology · 2026Article
- Maternal Obesity Reprograms Differentiation Trajectories of Fetal Hematopoietic Stem and Progenitor Cells Through Altered Inflammatory Signaling.bioRxiv : the preprint server for biology · 2026Article
- The long-term impact of obesity in pregnancy on offspring hypothalamic feeding pathways.Royal Society open science · 2025Review
- Developmental Programming of the Fetal Immune System by Maternal Western-Style Diet: Mechanisms and Implications for Disease Pathways in the Offspring.International journal of molecular sciences · 2024Review
- Maternal high fat diets: impacts on offspring obesity and epigenetic hypothalamic programming.Frontiers in genetics · 2023Review
- Female and male C57BL/6J offspring exposed to maternal obesogenic diet develop altered hypothalamic energy metabolism in adulthood.American journal of physiology. Endocrinology and metabolism · 2022Article
- Male Rat Offspring Are More Impacted by Maternal Obesity Induced by Cafeteria Diet than Females-Additive Effect of Postweaning Diet.International journal of molecular sciences · 2022Article
- Parental obesity-induced changes in developmental programming.Frontiers in cell and developmental biology · 2022Review
- Dietary curcumin supplementation promotes browning and energy expenditure in postnatal overfed rats.Nutrition & metabolism · 2021Article
- Maternal Obesity: A Focus on Maternal Interventions to Improve Health of Offspring.Frontiers in cardiovascular medicine · 2021Review
- Western Diet Consumption During Development: Setting the Stage for Neurocognitive Dysfunction.Frontiers in neuroscience · 2021Review
- Early life overnutrition impairs plasticity of non-neuronal brainstem cells and drives obesity in offspring across development in rats.International journal of obesity (2005) · 2020Article
- Article
- Perinatal exposure to maternal obesity: Lasting cardiometabolic impact on offspring.Prenatal diagnosis · 2020Review
- Interleukin 1 Receptor 1 Knockout and Maternal High Fat Diet Exposure Induces Sex-Specific Effects on Adipose Tissue Adipogenic and Inflammatory Gene Expression in Adult Mouse Offspring.Frontiers in physiology · 2020Article
- Priming of Hypothalamic Ghrelin Signaling and Microglia Activation Exacerbate Feeding in Rats' Offspring Following Maternal Overnutrition.Nutrients · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence from epidemiological, clinical, and experimental studies have clearly shown that disease risk in later life is increased following a poor early life environment, a process preferentially termed developmental programming. In particular, this work clearly highlights the importance of the nutritional environment during early development with alterations in maternal nutrition, including both under- and overnutrition, increasing the risk for a range of cardiometabolic and neurobehavioral disorders in adult offspring characterized by both adipokine resistance and obesity. Although the mechanistic basis for such developmental programming is not yet fully defined, a common feature derived from experimental animal models is that of alterations in the wiring of the neuroendocrine pathways that control energy balance and appetite regulation during early stages of developmental plasticity. The adipokine leptin has also received significant attention with clear experimental evidence that normal regulation of leptin levels during the early life period is critical for the normal development of tissues and related signaling pathways that are involved in metabolic and cardiovascular homeostasis. There is also increasing evidence that alterations in the epigenome and other underlying mechanisms including an altered gut-brain axis may contribute to lasting cardiometabolic dysfunction in offspring. Ongoing studies that further define the mechanisms between these associations will allow for identification of early risk markers and implementation of strategies around interventions that will have obvious beneficial implications in breaking a programmed transgenerational cycle of metabolic disorders.
Indexed as
Identifiers
What OpenQuestion holds
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.