3- tert -Butyl-4-hydroxyanisole Perturbs Differentiation of C3H10T1/2 Mesenchymal Stem Cells into Brown Adipocytes through Regulating Smad Signaling.
Wang X., Sun Z., Pei Y., Liu QS., Zhou Q., Jiang G.
Animal Study, published in Environ Sci Technol (2023) — 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
- Animal Study
- Journal
- Environ Sci Technol (2023)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 37481753
- DOI
- 10.1021/acs.est.3c02346
Abstract (original English)
3- tert -Butyl-4-hydroxyanisole (3-BHA), one of the most commonly used antioxidants in foodstuffs, has been identified as an environmental endocrine disruptor (EED) with obesogenic activity. Given the increasing concern on EED-caused dysfunction in lipid metabolism, whether 3-BHA could influence the development of brown adipocytes is worthy of being explored. In this study, the effect of 3-BHA on the differentiation of C3H10T1/2 mesenchymal stem cells (MSCs) into brown adipocytes was investigated. Exposure to 3-BHA promoted lipogenesis of the differentiated cells, as evidenced by the increased intracellular lipid accumulation and elevated expressions of adipogenic biomarkers, including peroxisome proliferator-activated receptor γ ( PPARγ ), Perilipin , Adiponectin , and fatty acid binding protein 4 ( FABP4 ). Surprisingly, the thermogenic capacity of the differentiated cells was compromised as a result of 3-BHA exposure, because neither intracellular mitochondrial contents nor expressions of thermogenic biomarkers, including uncoupling protein 1 ( UCP1 ), peroxisome proliferator-activated receptor γ coactivator 1α ( PGC1α ), cell-death-inducing DNA fragmentation factor α subunit-like effector A ( CIDEA ), and PR domain containing 16 ( PRDM16 ), were increased by this chemical. The underlying molecular mechanism exploration revealed that, in contrast to p38 MAPK, 3-BHA stimulati
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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