ArticleBiology of reproduction2022
Paternal obesity induces placental hypoxia and sex-specific impairments in placental vascularization and offspring metabolism†.
Article in Biology of reproduction, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 30 citations in OpenAlex.
- Paternal obesity decreases infant MSC mitochondrial functional capacity.American journal of physiology. Endocrinology and metabolism · 2024Trial
- Maternal High Fat Diet and Acute Viral Mimic Exposure Impact Placental Inflammation, Lipid Peroxidation and Cellular Proliferation-to-Death Ratio Across Mouse Pregnancy.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- Article
- A Review of the Effects of Maternal and Paternal Obesity on Neurodevelopmental Disorders and Related Neurobiology in Rodent and Human Offspring.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Environmentally-induced sperm RNAs shape placentation and fetal growth.Research square · 2026Article
- Maternal high-fat, high-sucrose diet-induced excess adiposity is linked to placental hypoxia and disruption of fetoplacental immune homeostasis in late gestation†.Biology of reproduction · 2025Article
- Dad's Diet Shapes the Future: How Paternal Nutrition Impacts Placental Development and Childhood Metabolic Health.Molecular nutrition & food research · 2025Review
- Intergenerational effects of cafeteria diet-induced obesity on metabolic and reproductive outcome in rats.Scientific reports · 2025Article
- Impact of Parental Time-Restricted Feeding on Offspring Metabolic Phenotypic Traits.International journal of biological sciences · 2025Article
- Review
- Article
- Paternal DDT exposure induces sex-specific programming of fetal growth, placenta development and offspring's health phenotypes in a mouse model.Scientific reports · 2024Article
- Review
- Prenatal paternal anxiety symptoms predict child DHEA levels and internalizing symptoms during adrenarche.Frontiers in behavioral neuroscience · 2023Article
- Sperm histone H3 lysine 4 tri-methylation serves as a metabolic sensor of paternal obesity and is associated with the inheritance of metabolic dysfunction.Molecular metabolism · 2022Article
- Paternal epigenetic influences on placental health and their impacts on offspring development and disease.Frontiers in genetics · 2022Review
- Metabolic Consequences of Gestational Cannabinoid Exposure.International journal of molecular sciences · 2021Review
- The Role of Cellular Stress in Intrauterine Growth Restriction and Postnatal Dysmetabolism.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paternal obesity predisposes offspring to metabolic dysfunction, but the underlying mechanisms remain unclear. We investigated whether this metabolic dysfunction is associated with changes in placental vascular development and is fueled by endoplasmic reticulum (ER) stress-mediated changes in fetal hepatic development. We also determined whether paternal obesity indirectly affects the in utero environment by disrupting maternal metabolic adaptations to pregnancy. Male mice fed a standard chow or high fat diet (60%kcal fat) for 8-10 weeks were time-mated with female mice to generate pregnancies and offspring. Glucose tolerance was evaluated in dams at mid-gestation (embryonic day (E) 14.5) and late gestation (E18.5). Hypoxia, angiogenesis, endocrine function, macronutrient transport, and ER stress markers were evaluated in E14.5 and E18.5 placentae and/or fetal livers. Maternal glucose tolerance was assessed at E14.5 and E18.5. Metabolic parameters were assessed in offspring at ~60 days of age. Paternal obesity did not alter maternal glucose tolerance but induced placental hypoxia and altered placental angiogenic markers, with the most pronounced effects in female placentae. Paternal obesity increased ER stress-related protein levels (ATF6 and PERK) in the fetal liver and altered hepatic expression of gluconeogenic factors at E18.5. Offspring of obese fathers were glucose intolerant and had impaired whole-body energy metabolism, with more pronounced effects in female offspring. Metabolic deficits in offspring due to paternal obesity may be mediated by sex-specific changes in placental vessel structure and integrity that contribute to placental hypoxia and may lead to poor fetal oxygenation and impairments in fetal metabolic signaling pathways in the liver.
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Registered trials
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