RSK2 facilitates beige fat formation through thermogenic and glycolytic pathways.
Cai Y., Chen JJ., He LF., Xu Y., Yang RQ., Yang ZC.
Animal Study, published in J Therm Biol (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
- J Therm Biol (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41610750
- DOI
- 10.1016/j.jtherbio.2026.104389
Abstract (original English)
Objectives Beige adipose tissue offers therapeutic potential for metabolic disorders. Notably, glycolytic beige adipocytes, which can be activated independently of β-adrenergic signaling, may provide unique advantages. This study aimed to investigate the role of p90 ribosomal S6 kinase-2 (RSK2) in both cold-induced and cold-independent glycolytic beige adipocyte formation. Methods We employed C57BL/6J mice subjected to cold exposure (4 °C) or high-fat diet (HFD) and analyzed adipose tissue for thermogenic and glycolytic markers. In vitro, subcutaneous adipose-derived stem cells (primary preadipocytes) were cultured at 28 °C to mimic cold exposure. RSK2 expression was manipulated via knockdown or overexpression to evaluate its functional role. Results Cold exposure upregulated uncoupling protein-1 (UCP1) and RSK2 in vivo, while HFD suppressed RSK2, UCP1, enolase 1 (ENO1), and pyruvate kinase isoform M2 (PKM2). In primary preadipocytes, cold exposure induced UCP1 and RSK2 expression and reduced triglyceride accumulation. RSK2 knockdown suppressed UCP1, acetyl-CoA carboxylase (ACC), and hormone-sensitive lipase (HSL) but increased carnitine palmitoyl transferase expression. It also reduced PKM2, ENO1, and lactate production under normothermic conditions, whereas RSK2 overexpression had opposite effects. High-glucose and high-insulin treatment decreased RSK2, glycolytic and thermog
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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