Department of Integrative Physiology and Bio-System Control, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan.
Biochem Biophys Res Commun. 2011 Jan 7;404(1):109-14. doi: 10.1016/j.bbrc.2010.11.076. Epub 2010 Nov 21.
Cyclic phosphatidic acid (cPA) is found in cells from slime mold to humans and has a largely unknown function. We previously reported that cPA significantly inhibited the lipid accumulation in 3T3-L1 adipocytes through inhibition of PPARγ activation. We find here that cPA reduced intracellular triglyceride levels and inhibited the phosphodiesterase 3B (PDE3B) expression in 3T3-L1 adipocytes. PPARγ activation in adipogenesis that can be blocked by treatment with cPA then participates in adipocyte function through inhibition of PDE3B expression. We also found the intracellular cAMP levels in 3T3-L1 adipocytes increased after exposure to cPA. These findings contribute to the participation of cPA on the lipolytic activity in 3T3-L1 adipocytes. Our studies imply that cPA might be a therapeutic compound in the treatment of obesity and obesity-related diseases.
环磷酸脂酸(cPA)存在于从黏菌到人类的细胞中,其功能很大程度上未知。我们之前的研究报道 cPA 通过抑制 PPARγ 的激活,显著抑制了 3T3-L1 脂肪细胞中的脂肪积累。我们在这里发现 cPA 降低了 3T3-L1 脂肪细胞中的细胞内甘油三酯水平,并抑制了磷酸二酯酶 3B(PDE3B)的表达。脂肪生成过程中 PPARγ 的激活可以通过 cPA 的处理来阻断,然后通过抑制 PDE3B 的表达参与脂肪细胞的功能。我们还发现,3T3-L1 脂肪细胞内的 cAMP 水平在接触 cPA 后增加。这些发现有助于 cPA 参与 3T3-L1 脂肪细胞的脂肪分解活性。我们的研究表明,cPA 可能是治疗肥胖和肥胖相关疾病的一种治疗化合物。