Curtis-Prior P B, Oblin A R, Tan S
Prostaglandins Med. 1979 Dec;3(6):361-6. doi: 10.1016/0161-4630(79)90028-4.
Plasma obtained from fasted rats provoked a dose-dependent stimulation of fat cell glycerol release and was able to inhibit also generation of prostaglandins E2 and F2 alpha from arachidonate, in vitro, over a very similar range of doses. It is proposed, therefore, that a plasmatic fat-mobilizing factor may act as an endogenous inhibitor of adipose tissue prostaglandin biosynthesis, mediating in the acute (long-term not precluded) regulation of adipose tissue lipolysis. The proposed mechanism of permissive effects of the plasmatic factor in reducing the effects of endogenously-generated inhibitory prostaglandins may be implicated in the development of obesity by reduced availability of the factor and thus reduced ability to utilize fat stores.
从禁食大鼠获得的血浆能引起脂肪细胞甘油释放的剂量依赖性刺激，并且在非常相似的剂量范围内，还能在体外抑制花生四烯酸生成前列腺素E2和F2α。因此，有人提出一种血浆脂肪动员因子可能作为脂肪组织前列腺素生物合成的内源性抑制剂，介导脂肪组织脂解的急性（长期影响也未排除）调节。血浆因子降低内源性生成的抑制性前列腺素作用的这种许可效应的 proposed机制，可能与肥胖的发生有关，因为该因子的可用性降低，从而利用脂肪储存的能力下降。
