Mechanism of adult primitive mesenchymal ST-13 preadipocyte differentiation.
Yajima Y., Sato M., Sumida M., Kawashima S.
Animal Study, published in Endocrinology (2003) — 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
- Endocrinology (2003)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 12746319
- DOI
- 10.1210/en.2002-220894
Abstract (original English)
Convincing evidence supports the idea that adipogenesis occurs throughout the life of organisms. However, little is known about the adipogenesis program for adult adipocytes. We examine this issue using mouse adult primitive mesenchymal ST-13 preadipocytes that express the peroxisome proliferator-activated receptor-gamma (PPARgamma) gene while in a predifferentiated state. The gene expression of PPARgamma was sustained throughout differentiation when ST-13 preadipocytes were induced to become adipocytes by a PPARgamma ligand. However, the differentiation of pluripotent C3H10T1/2 stem cells and 3T3-L1 embryonic fibroblastic cells was associated with enhanced expression of the PPARgamma gene. Immunoblotting analysis revealed that C3H10T1/2 and 3T3-L1 cells expressed low levels of PPARgamma1 from the early stage, and the amount increased during differentiation, whereas PPARgamma2 appeared at the late stage. In contrast, ST-13 preadipocytes expressed an appreciable amount of PPARgamma1 that significantly decreased on differentiation, and a small amount of PPARgamma2 appeared late in the differentiation process. Furthermore, the standard hormone cocktail containing dexamethasone, methylisobutylxanthine, and insulin induced an increase in PPARgamma1 protein only at the early stage, and a low level of PPARgamma2 protein appeared late in ST-13 cells. However, levels of both PPARgamma1
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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