Activating nuclear receptor subfamily 2 group F member 2 in adipocyte stem cells rescues beige adipocyte metabolism impaired by excess early-life omega-6 fatty acids.
Das S., Varshney RR., Farriester JW., Kyere-Davies G., Martinez AE., Hill KB.
Animal Study, published in Clin Nutr (2025) — 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
- Clin Nutr (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40527120
- PMCID
- PMC12257918
- DOI
- 10.1016/j.clnu.2025.06.003
- Citations
- 4
Abstract (original English)
Background and aims Developmental exposure to an elevated ratio of omega-6 (n6) to omega-3 (n3) fatty acids (FA) is linked to increased infant body fat and risk of future childhood obesity. We demonstrated in mice that the high n6/n3 developmental exposure reduced nuclear receptor subfamily 2 group F member 2 (NR2F2) in Adipocyte Stem Cells (ASCs), coincident with an altered ASC mitochondrial expression profile and increased white adipose accumulation in pups. This suggested that NR2F2-low ASCs might adopt a nutrient-storage phenotype. Here, we tested the hypothesis that NR2F2 is required in ASCs to undergo beige adipogenesis and metabolism needed during postnatal life for energy and thermogenesis. Methods C57BL/6J dams were randomized to either n6-rich or balanced n6/n3 control diets at the time of mating and underwent normal gestation and parturition. On postnatal day 12 (PND12), whole-body offspring metabolism was quantified by indirect calorimetry in conjunction with 13 C-palmitate and 13 C-glucose tracing. Inguinal fat pad ASCs were isolated by flow cytometry to assess adipocyte differentiation potential, global gene expression and proteomics, and mitochondrial oxidation. NR2F2 was transiently re-activated in vitro in ASCs with its ligand, 1-deoxysphingosine (1-DSO), and NR2F2 was ablated in ASCs ex vivo using homozygous floxed Nr2f2 pups to determine loss of function, ens
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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