Effects of obesity‐associated plasma markers on adipose stem cell function and epigenetic regulation
Authors' conclusion
In vitro leptin exposure enhanced CCL2 expression/secretion and increased KDM6A/KDM6B and EP300 transcription, highlighting how obesity-driven epigenetic mechanisms, including leptin-mediated pathways, disrupt ASC plasticity and perpetuate adipose tissue dysfunction, offering novel therapeutic targets for metabolic disease intervention.
Study context
- Population
- Male patients aged 30–50 years undergoing elective gastric or bariatric surgery; serum and visceral (omental) white adipose tissue (WAT) collected
- Participants
- 16 patients
- Outcome
- Correlations of BMI and obesity markers with ASC function and H3K27 epigenetic regulators
Main finding
As reported in the abstract
- ASCs from individuals with higher BMI showed slower proliferation, increased inflammatory profile and reduced adipogenic potential, with lower expression of key adipogenic genes
- H3K27 acetylase transcripts negatively correlated with adipogenesis regulators
- CCL2 and KDM6A expression higher in the group with obesity, as were CREBBP and EP300
- 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
Original publication
Effects of obesity‐associated plasma markers on adipose stem cell function and epigenetic regulation. Obesity (Silver Spring). Published 16 June 2025. doi:10.
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