The Long Noncoding RNA ΒFaar Promotes White Adipose Tissue Browning and Prevents Diet-Induced Obesity
Yang Y., Huang B., Sha B., Gao D., Qin Y., Li Z.
Animal Study, published in Adv Sci (Weinh) (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
- Adv Sci (Weinh) (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40548473
- PMCID
- PMC12463088
- DOI
- 10.1002/advs.202505545
- Citations
- 2
Abstract (original English)
The conversion of white adipose tissue (WAT) to brown adipose tissue (BAT) is a promising strategy for obesity treatment. It is previously identified βFaar as a conserved long noncoding RNA (lncRNA) regulator of islet β-cell function in individuals with obesity, but its effect on WAT browning is not well understood. In this study, it is discovered that βFaar expression in adipose tissue markedly decreases with the progression of obesity in both mice and humans. βFaar in adipose tissue reduces lipid droplet (LD) size in WAT and promotes a browning phenotype in inguinal WAT (iWAT), leading to the amelioration of high-fat diet (HFD)-induced obesity. These effects can be attributed to crosstalk between βFaar and proteins within the master regulatory pathways of LD formation and WAT browning, including RAS oncogene family 18 (RAB18) and interferon regulatory factor 4 (IRF4). Specifically, βFaar inhibits LD swelling by binding to RAB18 and promoting IRF4 nuclear translocation, increases uncoupling protein 1 (UCP1) transcription, and further induces iWAT browning by binding to karyopherin subunit alpha 6 (KPNA6). Together, these results demonstrate the critical roles of βFaar in regulating iWAT browning and preserving metabolic health; thus, βFaar may be a potential therapeutic target for management of obesity and related disorders.
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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