Effects of obesity-associated plasma markers on adipose stem cell function and epigenetic regulation.
Bispo AFS., de Jesus Simao J., Moraes MA., Abel ABM., Plata VTG., Telles MM.
Prospective Study with a reported sample of 16, published in Obesity (Silver Spring) (2025) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- 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
- Prospective Study
- Journal
- Obesity (Silver Spring) (2025)
- Country
- United States
- Reported sample size
- 16
- Source database
- PubMed
- PMID
- 40518865
- PMCID
- PMC12304845
- DOI
- 10.1002/oby.24321
- Citations
- 7
Abstract (original English)
Objective This study investigates the correlations between obesity-related plasma markers and epigenetic/inflammatory changes in white adipose tissue (WAT), focusing on adipose-derived stem cells (ASCs). We hypothesize that obesity modulates histone H3K27 marks, modified by demethylases (lysine-specific demethylase 6A and 6B [KDM6A/KDM6B]) and acetylases (CREB-binding protein [CREBBP]/histone acetyltransferase EP300), affecting ASC function. Methods Serum and visceral WAT (omental region) was collected from male patients (n = 16, 30-50 years old) undergoing elective gastric or bariatric surgery. BMI and obesity markers were correlated with changes in ASCs (transcript expression, proliferation, and secretion) using reverse transcriptase-polymerase chain reaction. Results ASCs from individuals with higher BMI exhibited slower proliferation, increased inflammatory profile, and reduced adipogenic potential, with lower expression of key adipogenic genes. H3K27 acetylase transcripts were also negatively correlated with adipogenesis regulators. Moreover, C-C motif chemokine 2 (CCL2) and KDM6A expression was higher in the group with obesity, as were CREBBP and EP300. Finally, leptin levels positively correlated with serum, WAT, and ASC CCL2 expression. In vitro, leptin exposure enhanced CCL2 expression/secretion and increased KDM6A/KDM6B and EP300 transcription. Conclusions In vitro le
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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