Richelsen B
Medical Department III, Aarhus amtssygehus, Tage Hansensgade, Denmark.
Biochem J. 1987 Oct 15;247(2):389-94. doi: 10.1042/bj2470389.
The regulation of PGE2 (prostaglandin E2) and PGI2 (prostaglandin I2; prostacyclin) formation was investigated in isolated adipocytes. The formation of both PGs was stimulated by various lipolytic agents such as isoproterenol, adrenaline and dibutyryl cyclic AMP. During maximal stimulation the production of PGE2 and PGI2 (measured as 6-oxo-PGF1 alpha) was 0.51 +/- 0.04 and 1.21 +/- 0.09 ng/2 h per 10(6) cells respectively. Thus PGI2 was produced in excess of PGE2 in rat adipocytes. The production of the PGs was inhibited by indomethacin and acetylsalicylic acid in a concentration-dependent manner. The half-maximal effective concentration of indomethacin was 328 +/- 38 nM and that of acetylsalicylic acid was 38.5 +/- 5.3 microM. The PGs were maximally inhibited by 70-75% after incubation for 2 h. In contrast with their effect on PG production, the two agents had a small potentiating effect on the stimulated lipolysis (P less than 0.05). The phospholipase inhibitors mepacrine and chloroquine inhibited both PG production and triacylglycerol lipolysis and were therefore unable to indicate whether the PG precursor, arachidonic acid, originates from phospholipids or triacylglycerols in adipocytes. Angiotensin II significantly (P less than 0.05) stimulated both PGE2 and PGI2 production in rat adipocytes without affecting triacylglycerol lipolysis. Finally, it was shown that PGE2 and PGI2 were also produced in human adipocytes, although in smaller quantities than in rat adipocytes. It is concluded that the production of PGs in isolated adipocytes is regulated by various hormones. Moreover, at least two separate mechanisms for PG production may exist in adipocytes: (1) a mechanism that is activated concomitantly with triacylglycerol lipolysis (and cyclic AMP) and (2) an angiotensin II-sensitive, but lipolysis (and cyclic AMP)-independent mechanism.
在分离的脂肪细胞中研究了前列腺素E2（PGE2）和前列腺素I2（PGI2；前列环素）生成的调节。两种前列腺素的生成均受到多种脂解剂的刺激，如异丙肾上腺素、肾上腺素和二丁酰环磷腺苷。在最大刺激下，PGE2和PGI2（以6-氧代-PGF1α衡量）的生成量分别为每10⁶个细胞0.51±0.04和1.21±0.09 ng/2小时。因此，大鼠脂肪细胞中PGI2的生成量超过PGE2。吲哚美辛和乙酰水杨酸以浓度依赖的方式抑制前列腺素的生成。吲哚美辛的半数有效浓度为328±38 nM，乙酰水杨酸的半数有效浓度为38.5±5.3 μM。孵育2小时后，前列腺素的生成被最大程度抑制70 - 75%。与它们对前列腺素生成的影响相反，这两种药物对刺激的脂解有轻微的增强作用（P＜0.05）。磷脂酶抑制剂米帕林和氯喹既抑制前列腺素的生成，也抑制三酰甘油的脂解，因此无法表明前列腺素前体花生四烯酸是来源于脂肪细胞中的磷脂还是三酰甘油。血管紧张素II显著（P＜0.05）刺激大鼠脂肪细胞中PGE2和PGI2的生成，而不影响三酰甘油的脂解。最后，研究表明人脂肪细胞中也生成PGE2和PGI2，尽管生成量比大鼠脂肪细胞中的少。结论是，分离的脂肪细胞中前列腺素的生成受多种激素调节。此外，脂肪细胞中可能存在至少两种独立的前列腺素生成机制：（1）一种与三酰甘油脂解（和环磷腺苷）同时被激活的机制；（2）一种对血管紧张素II敏感，但与脂解（和环磷腺苷）无关的机制。
