FTO Regulates Porcine Adipogenesis and Postnatal Survival of Cloned Embryos.

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

Abstract (original English)

The fat mass and obesity-associated gene (FTO), the first obesity-related gene and m6A demethylase, has well-defined roles in rodents but remains poorly understood in large mammals. Here, we combined siRNA-mediated knockdown, transcriptome sequencing, and bioinformatics to explore FTO function in porcine adipogenesis and embryo development. FTO silencing inhibited cell proliferation, promoted apoptosis, and suppressed adipogenic differentiation of adipose-derived mesenchymal stem cells (ADSCs) by downregulating key adipogenic genes (PPARγ, C/EBPα, FABP4, SCD, ACCα, LPL). Transcriptome analysis of CRISPR/Cas9-generated FTO-knockout fetal fibroblasts revealed altered pathways related to the cell cycle, senescence, apoptosis, and metabolism, including PI3K-Akt, Wnt, MAPK, and Apelin signaling. Using these knockout cells for somatic cell nuclear transfer (SCNT), we found that while FTO loss did not affect blastocyst formation, all cloned piglets carrying the mutation died postnatally. These results demonstrate that FTO is essential for porcine adipogenesis and postnatal survival of cloned embryos. The findings provided a new insight into the roles and mechanisms of FTO in fat metabolism and development in large mammals.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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