Tob2 inhibits peroxisome proliferator-activated receptor γ2 expression by sequestering Smads and C/EBPα during adipocyte differentiation
Takahashi A., Morita M., Yokoyama K., Suzuki T., Yamamoto T.
Animal Study, published in Mol Cell Biol (2012) — 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 Cell Biol (2012)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 23071089
- PMCID
- PMC3510534
- DOI
- 10.1128/mcb.00610-12
- Citations
- 21
Abstract (original English)
Adipogenesis is an important component of adipose tissue development and is critically related to obesity. A cascade of transcription factors is involved in adipogenesis, in which peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding proteins (C/EBPs) play pivotal roles. Bone morphogenetic proteins (BMPs) and Smad proteins are implicated in this cascade, although the precise regulatory mechanisms have yet to be elucidated. Here, we show that Tob2, a member of the Tob/BTG antiproliferative protein family, inhibits adipogenesis by interfering with Smad signaling. tob2 expression is downregulated in the white adipose tissue of high-fat diet-induced or genetically mutated obese mice. Consistent with this, tob2(-/-) mice exhibit increased adiposity with augmented expression of the genes encoding the type 1A BMP receptor (BMPR1A) and PPARγ2 as well as their target genes. We further show accelerated adipogenesis in primary tob2(-/-) preadipocytes. Furthermore, exogenously expressed Tob2 inhibits adipogenic differentiation of 3T3-L1 preadipocytes: the Tob2 protein suppresses PPARγ2 transcription by inhibiting BMP2-induced Smad1/5 phosphorylation through its interaction with Smad6 and by sequestering C/EBPα from the PPARγ2 promoter. Thus, Tob2 negatively regulates adipogenesis by inhibiting PPARγ2 expression.
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.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.