ArticleMolecular metabolism2015
Maternal high-fat diet and obesity compromise fetal hematopoiesis.
Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 65 citations in OpenAlex.
- Maternal Obesity Reprograms Differentiation Trajectories of Fetal Hematopoietic Stem and Progenitor Cells Through Altered Inflammatory Signaling.bioRxiv : the preprint server for biology · 2026Article
- Diet-induced obesity induces oxidative stress and enhances H3K4me3 levels, driving nonresolving inflammation and myelopoiesis in hematopoietic stem and progenitor cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Article
- Impact of PFOS Exposure on Murine Fetal Hematopoietic Stem Cells, Associated with Intrauterine Metabolic Perturbation.Environmental science & technology · 2025Article
- High-Fat Diet and Altered Radiation Response.Biology · 2025Review
- Maternal western-style diet alters Kupffer cell proportion leading to metabolic dysfunction-associated steatotic liver disease when challenged with western diet in adulthood.Frontiers in immunology · 2025Article
- Metabolic reprogramming of fetal hematopoietic stem and progenitor cells by maternal obesity.Frontiers in hematology · 2025Article
- The influence of high-fat diet and energy-restricted diet on hematopoietic stem cells: mechanisms and implications.Frontiers in immunology · 2025Review
- A Brief Historic Review of Research on Early Life Stress and Inflammation across the Lifespan.Neuroimmunomodulation · 2025Review
- Glucose intolerance as a consequence of hematopoietic stem cell dysfunction in offspring of obese mice.Molecular metabolism · 2024Article
- Developmental programming of tissue-resident macrophages.Frontiers in immunology · 2024Review
- Review
- Maternal diet alters long-term innate immune cell memory in fetal and juvenile hematopoietic stem and progenitor cells in nonhuman primate offspring.Cell reports · 2023Article
- Maternal obesity induced metabolic disorders in offspring and myeloid reprogramming by epigenetic regulation.Frontiers in endocrinology · 2023Review
- Maternal Western-style diet remodels the transcriptional landscape of fetal hematopoietic stem and progenitor cells in rhesus macaques.Stem cell reports · 2022Article
- Epigenetic and Transcriptomic Programming of HSC Quiescence Signaling in Large for Gestational Age Neonates.International journal of molecular sciences · 2022Article
- The Role ofFrontiers in medicine · 2022Article
- Maternal obesity and the impact of associated early-life inflammation on long-term health of offspring.Frontiers in cellular and infection microbiology · 2022Review
- Article
- A Glimpse at the Size of the Fetal Liver-Is It Connected with the Evolution of Gestational Diabetes?International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveRecent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high-fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity.
methodsWe used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high-fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system.
resultsMaternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration.
conclusionsOur data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment.
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