Alteration by 2,3,7,8-Tetrachlorodibenzo-p-dioxin of CCAAT/enhancer binding protein correlates with suppression of adipocyte differentiation in 3T3-L1 cells.
Liu PC., Phillips MA., Matsumura F.
Animal Study, published in Mol Pharmacol (1996) — 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
- Mol Pharmacol (1996)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 8649359
Abstract (original English)
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related compounds elicit multiple effects on the function of adipose tissue and adipogenic cell lines, including the suppression of adipocyte differentiation. We began to examine the mechanism by which TCDD inhibits differentiation of the established preadipocyte cell line 3T3-L1. Examination of the expression of several early marker genes of preadipocyte differentiation through Northern blot analysis and of differentiation-dependent mitosis showed that TCDD did not interfere with the earliest known responses of preadipocytes to inducers of differentiation. Analysis of mRNA for three isoforms of the CCAAT/enhancer binding protein (C/EBP) revealed that TCDD (5 nM) selectively inhibited the induction of C/EBP alpha mRNA but did not block the induction of C/EBP beta and C/EBP delta in response to differentiation inducers. The differentiation-dependent induction of PPAR gamma mRNA was also blocked by TCDD. Immunoblot analysis with specific antibodies to each C/EBP isoform demonstrated that the levels of C/EBP delta and C/EBP beta protein were rapidly induced (by day 1) and then abrogated by day 4 and 8, respectively, in solvent-treated (control) cells. In TCDD-treated cells, however, the levels of C/EBP beta and C/EBP delta protein persisted at these time points. In contrast, C/EBP alpha protein was markedly suppressed by TCDD in conco
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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