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Cited by 23Epigenetics and DNA MethylationBirth, Development, and HealthGenetic Syndromes and Imprinting

Paternal High-Fat Diet Affects Weight and DNA Methylation of Their Offspring

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Haberman, Michal, Menashe, Tzlil, Cohen, Nir, Kisliouk, Tatiana, Yadid, Tam, Marco, Asaf, Meiri, Noam, Weller, Aron·2024·Scientific Reports
DOI 10.1038/s41598-024-70438-yPMC PMC11349951
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Abstract

Obesity poses a public health threat, reaching epidemic proportions. Our hypothesis suggests that some of this epidemic stems from its transmission across generations via paternal epigenetic mechanisms. To investigate this possibility, we focused on examining the paternal transmission of CpG methylation. First-generation male Wistar rats were fed either a high-fat diet (HF) or chow and were mated with females fed chow. We collected sperm from these males. The resulting offspring were raised on a chow diet until day 35, after which they underwent a dietary challenge. Diet-induced obese (DIO) male rats passed on the obesogenic trait to both male and female offspring. We observed significant hypermethylation of the Pomc promoter in the sperm of HF-treated males and in the hypothalamic arcuate nucleus (Arc) of their offspring at weaning. However, these differences in Arc methylation decreased later in life. This hypermethylation is correlated with increased expression of DNMT3B. Further investigating genes in the Arc that might be involved in obesogenic transgenerational transmission, using reduced representation bisulfite sequencing (RRBS) we identified 77 differentially methylated regions (DMRs), highlighting pathways associated with neuronal development. These findings support paternal CpG methylation as a mechanism for transmitting obesogenic traits across generations.

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  • Both maternal and paternal nutritional environments before and during conception can profoundly influence offspring metabolic programming through heritable epigenetic mechanisms.

    “Together, these findings demonstrate that both maternal and paternal nutritional environments before and during conception can profoundly influence offspring metabolic programming through heritable epigenetic mechanisms.”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [179]

    The Introduction (page unavailable) reports offspring methylation changes after maternal high-fat feeding, and the Discussion (page unavailable) reports paternal transmission of obesity-related traits and methylation changes in sperm and offspring. But the Introduction says maternal transmission could reflect direct effects during development rather than inheritance through gametes, while the Discussion describes the paternal mechanism as a possibility. The source therefore does not demonstrate heritable epigenetic mechanisms for both parents as the claim states. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Offspring of these males displayed altered POMC mRNA expression and higher leptin levels, even when fed a control diet (HF-CH), indicating that paternal HFD exposure induced stable epigenetic modifications transmitted through sperm.

    “Offspring of these males displayed altered POMC mRNA expression and higher leptin levels, even when fed a control diet (HF–CH), indicating that the paternal HFD exposure induced stable epigenetic modifications transmitted through sperm.”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [179]

    The Results section reports significantly altered Pomc mRNA expression in HF–CH offspring, but describes their higher leptin level relative to CH–CH offspring as a non-significant tendency (p = 0.06). The paper finds altered methylation in fathers’ sperm and young offspring, yet its Discussion says offspring Pomc methylation differences diminished by PND 60 and frames germline transmission as a possibility, not an established stable mechanism. No page numbers are available in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • In a mouse model, males fed an HFD exhibited differential methylation at 24 CpG sites in the POMC promoter region of sperm DNA, with methylation levels correlating positively with body weight.

    “Haberman et al. showed that males fed an HFD exhibited differential methylation at 24 CpG sites in the POMC promoter region of sperm DNA, with methylation levels correlating positively with body weight [179].”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [179]

    The Results passage on spermatozoa reports that 24 Pomc promoter CpG sites were analyzed, but significantly higher methylation in high-fat-fed males occurred at eight sites, not all 24. It also reports a positive correlation between methylation across the 24 sites and body weight. The animals were rats, not mice. (LLM, conf=0.93)

    Experimental — accuracy not yet measured

  • Parental health and diet, not only during pregnancy but also prior to conception, play a crucial role in shaping disease susceptibility across generations.

    “The concept of transgenerational inheritance thus expands the traditional view of fetal programming, emphasizing that parental health and diet—not only during pregnancy but also prior to conception—play a crucial role in shaping disease susceptibility across generations [73,169,175,177,178,179].”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [179]

    The Introduction describes paternal diet and obesity before conception as possible routes of inherited obesity risk, distinct from maternal effects during pregnancy. The Discussion reports both maternal and paternal associations with offspring obesity, but this paper’s own experiment tests paternal high-fat diet in rats. It does not establish the broader claim about parental health and diet shaping disease susceptibility generally across generations. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Methylation changes in the POMC promoter persisted in the sperm of F1 males, confirming a transgenerational inheritance of paternal epigenetic marks.

    “Importantly, methylation changes in the POMC promoter persisted in the sperm of F1 males, confirming a transgenerational inheritance of paternal epigenetic marks [179].”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [179]

    The Results (page not supplied) report Pomc-promoter hypermethylation in F0 males’ sperm and in the arcuate nucleus of their F1 offspring, not in F1 males’ sperm. The Discussion (page not supplied) describes transgenerational transmission of obesogenic traits as a possibility; these findings do not confirm persistence of paternal epigenetic marks in F1 sperm. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

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Authors
Haberman, M., Menashe, T., Cohen, N., Kisliouk, T., Yadid, T., Marco, A., Meiri, N., & Weller, A.
Affiliations
  • Bar-Ilan University (IL)
  • Agricultural Research Organization (IL)
  • Hebrew University of Jerusalem (IL)
Corresponding author
Meiri, Noam
ORCID
Venue
Scientific Reports
Publisher
Springer Science and Business Media LLC
Published
2024-08-27
Volume
14
Issue
1
Pages
19874-19874
ISSN
2045-2322 (ISSN-L)
DOI
10.1038/s41598-024-70438-y
PMC
PMC11349951
OpenAlex
W4401906057
Cited by
23
References
2
Citations by year
2026: 8 · 2025: 14 · 2024: 1
FWCI
3.13
Type
journal article
Language
en
Open access
Licence
Locations
  • Scientific Reports (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Israel Science Foundation (1781/16)
  • Ministry of Science and Technology, Israel (3-15689)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
Keywords
transgenerational epigenetic inheritance, DNA methylation, obesity, hypothalamic arcuate nucleus, DNMT3B, differentially methylated regions, diet-induced obesity, Wistar rats, neuronal development
MeSH terms
Paternal Inheritance, DNA Methyltransferase 3B, Animals, Arcuate Nucleus of Hypothalamus, Body Weight, DNA (Cytosine-5-)-Methyltransferases, Female, Male, Obesity, Pro-Opiomelanocortin, Promoter Regions, Genetic, Spermatozoa, Rats, Wistar, CpG Islands, DNA Methylation, Epigenesis, Genetic, Rats, Diet, High-Fat

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