Obese Adipose Tissue Extracellular Vesicles Activate Mitochondrial Fatty Acid β-oxidation to Drive Colonic Stemness.
Haque PS., Goodman D., Kuusivuori-Robinson T., Coughlan C., Delgado-Deida Y., Onyiah JC.
Prospective Study, published in Cell Mol Gastroenterol Hepatol (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
- Cell Mol Gastroenterol Hepatol (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40122519
- DOI
- 10.1016/j.jcmgh.2025.101504
Abstract (original English)
Patients with obesity and mouse models of obesity exhibit abnormalities in intestinal epithelial cells, including enhanced stemness. Adipose tissue (AT) is the largest endocrine organ secreting cytokines, hormones, and extracellular vesicles (EVs). Here, we characterized EV protein cargo from obese and non-obese AT and demonstrate the role of obese adipose-derived EVs in enhancing colonic stemness. EVs were isolated from visceral AT from mice fed high-fat diet to induce obesity or control matched-diet. EV cargo was characterized by unbiased proteomics. Mouse colonoids were treated with EVs and analyzed for fatty acid β-oxidation (FAO), expression of stem marker genes, stem function, and β-catenin expression and acetylation. Mice deficient in adipocyte-specific Tsg101 expression were generated to alter adipocyte EV protein cargo, and colonic stemness was measured. EVs secreted from obese visceral AT (Ob EVs) were significantly enriched with acyl-CoA dehydrogenase long chain (ACADL), an initiator enzyme of FAO. Compared with non-obese EVs, colonoids treated with Ob EVs exhibited increased exogenous ACADL protein expression, FAO, growth, persistence of stem/progenitor function, and increased β-catenin protein expression and acetylation that was abolished by FAO inhibition. Mice deficient in adipocyte-specific Tsg101 expression exhibited Ob EVs with altered protein expression profi
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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