The mechanism by which methylase METTL3 affects intramuscular fat deposition
Yu B., Li K., Li X., Zhang J.
Animal Study, published in Poult Sci (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Poult Sci (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41780492
- PMCID
- PMC12969675
- DOI
- 10.1016/j.psj.2026.106670
Abstract (original English)
N 6 -methyladenosine (m 6 A) is a critical epigenetic modification that regulates lipid metabolism; however, its role in adipogenesis in chickens remains unclear. Here, we demonstrated that the m 6 A methylase METTL3 shows significant differences at the key stage of chicken development, and its expression in the breast muscle is significantly higher than in other tissues. Furthermore, METTL3 expression gradually decreases during the differentiation of both intramuscular preadipocytes (IMPA) and abdominal preadipocytes (APA). Gain- and loss-of-function assays demonstrated that METTL3 overexpression significantly inhibited the proliferation and differentiation of IMPA and APA cells, whereas METTL3 knockdown exerted the opposite effect. Combined with m 6 A sequencing (m 6 A-seq), we identified significant enrichment of m 6 A modification within the 3' untranslated region (3'UTR) of PCYT1A mRNA, indicating it as a direct modification target of METTL3. Mechanistically, METTL3 knockdown reduced m 6 A methylation of PCYT1A, consequently enhancing PCYT1A mRNA stability and expression. This upregulation of PCYT1A promoted adipogenic differentiation in both IMPA and APA. Our study elucidates the functional mechanism by which METTL3-mediated m 6 A modification regulates lipid deposition through modulating PCYT1A expression, thereby identifying novel molecular targets for investigating adi
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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