Fain J N, Kanu A, Bahouth S W, Cowan G S M, Hiler M L, Leffler C W
Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, TN, USA.
Prostaglandins Leukot Essent Fatty Acids. 2002 Dec;67(6):467-73. doi: 10.1054/plef.2002.0430.
The present studies were designed to investigate the sites of PGE(2), prostacyclin and leptin formation in human adipose tissue. Most of the PGE(2) and prostacyclin formation by adipose tissue explants from obese humans after 48 h in primary culture was due to blood vessels and other tissues not digested by collagenase. However, there was appreciable PGE(2) formation by adipocytes over a 48 h incubation and leptin formation was only seen in adipocytes. An increase in COX-2 immunoreactive protein was also seen after incubation of isolated human adipocytes for 48 h. The release of PGE(2) by adipocytes incubated for 48 h was about 4% that by intact adipose tissue explants while the release of prostacyclin was about 1.5% that by tissue. However, in a different experimental design where PGE(2) formation was measured over 2 h in the presence of 20 microM arachidonic acid the formation of PGE(2) by adipocytes after 48 h prior incubation in primary culture was 38% of that by tissue explants. Dexamethasone enhanced leptin release by adipocytes while inhibiting PGE(2) release and COX-2 up-regulation. The mechanisms involved in up-regulation of COX-2 activity during primary culture of adipocytes and the inhibition of this by dexamethasone do not appear to involve p38 MAPK or p42-44 MAPK. Interleukin I(beta) further enhanced PGE(2) formation by adipocytes but did not affect leptin formation. In conclusion, these data indicate that leptin release is exclusively a function of adipocytes while prostanoids are made by both adipocytes and the other cells present in human adipose tissue
本研究旨在探究前列腺素E2（PGE2）、前列环素和瘦素在人体脂肪组织中的生成部位。肥胖人群脂肪组织外植体在原代培养48小时后，其产生的大部分PGE2和前列环素是由未被胶原酶消化的血管和其他组织所致。然而，脂肪细胞在48小时的孵育过程中会产生可观的PGE2，且仅在脂肪细胞中可见瘦素的生成。分离的人体脂肪细胞孵育48小时后，COX-2免疫反应性蛋白也有所增加。孵育48小时的脂肪细胞释放的PGE2约为完整脂肪组织外植体的4%，而前列环素的释放量约为组织的1.5%。然而，在另一种实验设计中，在20微摩尔花生四烯酸存在的情况下测量2小时内PGE2的生成，原代培养中预先孵育48小时的脂肪细胞产生的PGE2是组织外植体的38%。地塞米松可增强脂肪细胞释放瘦素，同时抑制PGE2释放和COX-2上调。脂肪细胞原代培养过程中COX-2活性上调以及地塞米松对此的抑制所涉及的机制似乎不涉及p38丝裂原活化蛋白激酶（MAPK）或p42 - 44 MAPK。白细胞介素1β（IL-1β）进一步增强脂肪细胞生成PGE2，但不影响瘦素生成。总之，这些数据表明瘦素的释放完全是脂肪细胞的功能，而类前列腺素由人体脂肪组织中的脂肪细胞和其他细胞共同产生
