The KLF2 transcription factor does not affect the formation of preadipocytes but inhibits their differentiation into adipocytes.
Wu J., Srinivasan SV., Neumann JC., Lingrel JB.
Animal Study, published in Biochemistry (2005) — 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
- Biochemistry (2005)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 16101293
- DOI
- 10.1021/bi050166i
Abstract (original English)
Kruppel-like transcription factor 2 (KLF2), a critical gene for mouse embryogenesis, was recently identified as an inhibitor of adipogenesis. However, it is still unknown whether KLF2 is a natural repressor of adipocyte differentiation and if KLF2 affects the formation of preadipocytes. It may also be important for preadipocyte formation, as KLF2 is crucial for lung development and blood vessel formation. In this study, we show that differentiation of preadipocytes not only results in a concomitant decrease in the levels of KLF2 protein but also significantly reduces KLF2 promoter activity. We have generated tet-responsive lines of 3T3L1 that express physiological levels of KLF2 and show that reexpression of KLF2 prevents preadipocyte differentiation, thereby confirming the inhibition of adipogenesis by KLF2, partially via the restoration of Pref-1. In addition, we studied the contribution of KLF2-negative cells to the formation and subsequent differentiation of preadipocytes. We demonstrate that embryoid bodies derived from KLF2(-)(/)(-) ES cells can differentiate into adipocytes as evidenced by the accumulation of lipids and expression of several biochemical markers. Moreover, mouse embryonic fibroblasts (MEFs) derived from KLF2(-)(/)(-) mouse embryos differentiate efficiently into adipocytes. Interestingly, quantification of lipid accumulation in MEFs indicated that KLF2(-)(
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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