RUNX1T1 enhances intramuscular fat deposition in pigs through promoting fibro-adipogenic progenitors adipogenesis via PI3K-AKT and MAPK signaling pathways.
Zhang X., Xu J., Jiang Y., Zhao C., Yang C., Chen C.
Animal Study, published in Biochem Biophys Res Commun (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
- Biochem Biophys Res Commun (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41905166
- DOI
- 10.1016/j.bbrc.2026.153624
Abstract (original English)
Enhancing intramuscular fat (IMF) content in fast-growing pig breeds is a key breeding objective for higher pork quality. However, the specific molecular mechanisms underlying this trait remain poorly understood. Here, we measured the IMF content of 10 Duroc pigs and found that they can be classified into Low and High IMF groups (2.56 ± 0.64% vs 5.88 ± 1.38%). RNA-seq of longissimus dorsi muscle (LDM) from Low and High IMF pigs was performed, and 1166 up-regulated genes were identified in High IMF pigs (Fold change >1.5, P < 0.05). Gene Ontology analysis revealed that 12 genes were assigned known functions in the adipocyte differentiation pathway. Among these, Runt-related transcription factor 1 translocation partner 1 (RUNX1T1) gene was selected for further investigation due to its higher expression in the High IMF group. We isolated fibro-adipogenic progenitors (FAPs) and found that RUNX1T1 overexpression significantly enhanced adipogenic differentiation, as evidenced by increased lipid droplet formation and elevated expression of adipogenesis-related markers (P < 0.05). Conversely, the silencing of RUNX1T1 inhibited these differentiation phenotypes (P < 0.05). Mechanistically, RUNX1T1 regulated adipogenesis positively through both the PI3K-AKT and MAPK/ERK1/2 signaling pathways (P < 0.05). In conclusion, our results establish RUNX1T1 as a key regulator of IMF deposition in p
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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