Peroxisome Proliferator-activated Receptor γ Is Not Associated with Adipogenesis in Female Mice
Michung Yoon, Sunhyo Jeong
Abstract
Michung Yoon, Sunhyo Jeong
Abstract
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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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.
Key concepts: Troglitazone, Adipogenesis, Adipose tissue, Adipocyte, Endocrinology, Internal medicine, Peroxisome proliferator-activated receptor, Biology