Yu Y H, Wu S C, Cheng W T K, Mersmann H J, Ding S T
Department of Animal Science and Technology/Institute of Biotechnology, National Taiwan University, Taipei 106, Taiwan.
J Anim Sci. 2008 Jan;86(1):64-72. doi: 10.2527/jas.2007-0399. Epub 2007 Sep 18.
Peroxisome proliferator-activated receptor gamma (PPARgamma) plays a critical role in regulating adipogenesis. The expression of peroxisome proliferator-activated receptor delta (PPARdelta) precedes that of PPARgamma during adipocyte differentiation in rodents. The current experiment was designed to study the function of porcine PPARdelta and the interaction of PPARdelta and PPARgamma in adipocyte differentiation. Inhibition of myogenesis was observed in mouse myoblasts expressing porcine PPARdelta, similar to myoblasts expressing PPARgamma. Treatment of myoblasts expressing PPARdelta with ligands for both PPARdelta and PPARgamma enhanced lipogenesis and adipogenesis to a greater extent than treatment with a PPARgamma ligand alone, suggesting that both genes were involved in regulating lipogenesis and adipogenesis. The ability to transdifferentiate myoblasts into adipocytes was decreased in myoblasts coexpressing PPARdelta with either wild type or mutated PPARgamma (Ser 112 was mutated to Ala; the mutated PPARgamma is more active than the wild type) compared with myoblasts expressing PPARgamma alone. Adipocyte differentiation in myoblasts coexpressing PPARdelta and mutated PPARgamma was greater than in myoblasts coexpressing PPARdelta and wild type PPARgamma, confirming that Ser 112 is important for the function of PPARgamma. Taken together, our results demonstrate that overexpression of PPARdelta inhibits myotube formation and also enhances adipocyte differentiation. However, the complexity and interaction of PPARdelta and PPARgamma in adipogenesis are not clearly understood.
过氧化物酶体增殖物激活受体γ（PPARγ）在调节脂肪生成中起关键作用。在啮齿动物的脂肪细胞分化过程中，过氧化物酶体增殖物激活受体δ（PPARδ）的表达先于PPARγ。当前实验旨在研究猪PPARδ的功能以及PPARδ与PPARγ在脂肪细胞分化中的相互作用。在表达猪PPARδ的小鼠成肌细胞中观察到了成肌抑制，这与表达PPARγ的成肌细胞类似。用PPARδ和PPARγ的配体处理表达PPARδ的成肌细胞，比单独用PPARγ配体处理能更大程度地增强脂肪生成和脂肪形成，这表明这两个基因都参与调节脂肪生成和脂肪形成。与单独表达PPARγ的成肌细胞相比，共表达PPARδ与野生型或突变型PPARγ（Ser112突变为Ala；突变型PPARγ比野生型更活跃）的成肌细胞将成肌细胞转分化为脂肪细胞的能力降低。共表达PPARδ和突变型PPARγ的成肌细胞中的脂肪细胞分化大于共表达PPARδ和野生型PPARγ的成肌细胞，证实Ser112对PPARγ的功能很重要。综上所述，我们的结果表明PPARδ的过表达抑制肌管形成，同时也增强脂肪细胞分化。然而，PPARδ与PPARγ在脂肪生成中的复杂性和相互作用尚不清楚。
