Donor-specific response of visceral adipocytes differentiated from human adipose-derived mesenchymal stem cells to branched-chain alpha-keto acid (BCKA) dehydrogenase activation.
Supruniuk E., Mikłosz A., Łukaszuk B., Baranowski M., Paszko A., Szczerbiński Ł.
Laboratory Study on Face & Skin, published in Biomed Pharmacother (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
- Laboratory Study
- Journal
- Biomed Pharmacother (2025)
- Country
- France
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40752427
- DOI
- 10.1016/j.biopha.2025.118426
Abstract (original English)
Aims The causal role of branched-chain amino acids (BCAAs) and their transamination derivatives (branched-chain α-ketoacids, BCKAs) was observed in the progression of obesity and its metabolic complications. In the study, we aimed to stimulate BCAA catabolic flux with an inhibitor of BCKA dehydrogenase kinase (i.e., BT2) to explore metabolic consequences using visceral ADMSCs, obtained from non-obese men and men with obesity, and differentiated to adipocytes. Materials and methods ADMSCs metabolism was assessed using real-time PCR, Western Blot, Ultra-High Performance Liquid Chromatography, Gas-Liquid Chromatography, Seahorse analysis, liquid scintillation counting, flow cytometry, immunofluorescence and spectrophotometric assays. Results We report that obesity was associated with the redistribution of fatty acid transporters among a higher number of adipocytes (higher number of CD36/SR-B2 and FATP4 positive cells), but at the same time lowered surface abundance of transporters per cell (CD36/SR-B2, FATP1, FATP4, FABPpm). Despite that, the metabolic consequences of BT2 administration were strictly associated with the donor-specific inherent cellular properties, what enabled a differentiation of two adipocyte subpopulations with low and high metabolic activity. BT2 effects were more profound in the latter group, wherein pro-lipolytic and β-oxidation-related markers were upregula
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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