Peroxisome Proliferator-activated Receptor γ Is Not Associated with Adipogenesis in Female Mice

저작시기 2008.09 |등록일 2009.04.22 파일확장자어도비 PDF (pdf) | 8페이지 | 가격 6,000원
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* 본 문서는 배포용으로 복사 및 편집이 불가합니다.

서지정보

발행기관 : 대한의생명과학회 수록지정보 : 대한의생명과학회지 / 14권 / 3호
저자명 : Michung Yoon, Sunhyo Jeong

목차

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
Acknowledgements
REFERENCES

한국어 초록

The peroxisome proliferator-activated receptor γ (PPARγ) plays a central role in adipogenesis and lipid storage. The PPARγ ligands, thiazolidinediones (TZDs), enhance in vitro adipogenesis in several cell types, but the role of the TZDs on in vivo adipogenesis is still poorly understood. To investigate how PPARγ ligand troglitazone regulates adipogenesis in female mice, we examined the effects of the troglitazone on adipose tissue mass, morphological changes of adipocytes, and the expression of PPARγ target and adipocyte-specific genes in low fat diet-fed female C57BL/6 mice. Administration of troglitazone for 13 weeks did not change body and total white adipose tissue weights compared with control mice. Troglitazone treatment also did not cause a significant decrease in the average size of adipocytes in parametrial adipose tissue although it is reported to increase the number of small adipocytes in male animals. Troglitazone did not affect the mRNA expression of PPARγ and its target genes as well as adipocyte-specific genes in parametrial adipose tissue. These results suggest that PPARγ does not seem to be associated with adipogenesis in females with functioning ovaries and that its inability to induce adipogenesis may be due to sex-related factors.

영어 초록

The peroxisome proliferator-activated receptor γ (PPARγ) plays a central role in adipogenesis and lipid storage. The PPARγ ligands, thiazolidinediones (TZDs), enhance in vitro adipogenesis in several cell types, but the role of the TZDs on in vivo adipogenesis is still poorly understood. To investigate how PPARγ ligand troglitazone regulates adipogenesis in female mice, we examined the effects of the troglitazone on adipose tissue mass, morphological changes of adipocytes, and the expression of PPARγ target and adipocyte-specific genes in low fat diet-fed female C57BL/6 mice. Administration of troglitazone for 13 weeks did not change body and total white adipose tissue weights compared with control mice. Troglitazone treatment also did not cause a significant decrease in the average size of adipocytes in parametrial adipose tissue although it is reported to increase the number of small adipocytes in male animals. Troglitazone did not affect the mRNA expression of PPARγ and its target genes as well as adipocyte-specific genes in parametrial adipose tissue. These results suggest that PPARγ does not seem to be associated with adipogenesis in females with functioning ovaries and that its inability to induce adipogenesis may be due to sex-related factors.

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