Curtis-Prior P B
Lancet. 1975 Apr 19;1(7912):897-9. doi: 10.1016/s0140-6736(75)91690-6.
In metabolic obesity energy in triglyceride stores is not readily accessible, and lipolysis to free fatty acid and glycerol seems to be somehow restrained. In the normal situation, there is a balance between a forward reaction via cyclic A.M.P. ending in lipolysis and a negative-feedback mechanism in which prostaglandins participate. In metabolic obesity there may be a biochemical error leading to overproduction of prostaglandins; as a result the forward reaction is overwhelmed and lipolysis does not take place. Since prostaglandin antagonists and inhibitors of prostaglandin synthesis are known, this hypothesis is not without therapeutic interest.
在代谢性肥胖中,甘油三酯储存中的能量不易获取,脂肪分解为游离脂肪酸和甘油的过程似乎受到某种程度的抑制。在正常情况下,通过环磷酸腺苷(cAMP)的正向反应最终导致脂肪分解,与前列腺素参与的负反馈机制之间存在平衡。在代谢性肥胖中,可能存在生化错误导致前列腺素过度产生;结果正向反应占主导,脂肪分解无法发生。由于已知前列腺素拮抗剂和前列腺素合成抑制剂,这一假说具有一定的治疗意义。