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前列腺素与肥胖

Prostaglandins and obesity.

作者信息

Curtis-Prior P B

出版信息

Lancet. 1975 Apr 19;1(7912):897-9. doi: 10.1016/s0140-6736(75)91690-6.

Abstract

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.

摘要

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。

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