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초록·키워드 목차

Adipogenesis is a complex sequence of events that culminates in the differentiation of fibroblast-like preadipocytes into specialized lipid-filled adipocytes and also involves a cascade of expression of many transcription factors such as peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding proteins (C/EBPs). PPARγ and C/EBPs transcriptionally transactivate adipocyte specific genes, including fatty acid transport protein (FAT/CD36) and leptin. To determine whether 17β-estradiol modulates C/EBPα actions on adipogenesis in high fat diet-fed female ovariectomized (OVX) C57BL/6 mice, mice were treated with 17β-estradiol for 7 days and the effects of 17β-estradiol on adipose tissue mass and expression of adipocyte specific gene as well as C/EBPα were measured. Compared to vehicle-treated OVX control mice, OVX mice treated with 17β-estradiol for 7 days had lower adipose tissue weights that were similar to weights in high fat diet-fed sham-operated (Sham) mice. OVX mice showed the increased expression of C/EBPα mRNA compared with Sham mice. However, 17β-estradiol treatment in OVX mice inhibited OVX induced-C/EBPα activation, indicating that 17β-estradiol may act as an inhibitor of C/EBPα action. Moreover, 17β-estradiol decreased mRNA levels of adipocyte marker genes, such as lipoprotein lipase, FAT/CD36 and leptin, to levels in Sham mice. These results suggest that down-regulation of adipogenesis by 17β-estradiol may be due to reduced adipose C/EBPα activities in female OVX C57BL/6 mice. #17β-estradiol #C/EBPα #Adipogenesis #Female mice

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
Acknowledgements
REFERENCES

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