ArticleCellular and molecular gastroenterology and hepatology2025
Obese Adipose Tissue Extracellular Vesicles Activate Mitochondrial Fatty Acid β-oxidation to Drive Colonic Stemness.
Article in Cellular and molecular gastroenterology and hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Secretion of Extracellular Vesicles Into the Mesenteric Lymph During Fasting and Lipid Absorption.Journal of extracellular biology · 2026Article
- Pathophysiological Roles of Obesity-Induced Alterations in Extracellular Vesicles Derived from Adipose Tissue and Adipocytes.Current obesity reports · 2026Review
- Extracellular vesicles and acetylation: reciprocal regulation in disease progression.Frontiers in immunology · 2026Review
- Fa(s)t Delivery: How Extracellular Vesicles Fuel Stem Cell Metabolism.Cellular and molecular gastroenterology and hepatology · 2025Article
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Authors and funding
8 authors.
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Abstract
BACKGROUND &
aimsPatients 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.
methodsEVs 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.
resultsEVs 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 profiles and were protected from obesity-induced enhanced colonic stemness.
conclusionsThe contents of Ob EVs are poised to fuel FAO and to promote obesity-induced stemness in the colon. Alteration of metabolism is a key mechanism of adipose-to-intestinal tissue communication elicited by EVs, thereby influencing basal colonic stem cell homeostasis during obesity.
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