EFFECTS OF INSULIN AND DEXAMETHASONE ON LIPOPROTEIN-LIPASE IN HUMAN ADIPOSE-TISSUE
EFFECTS OF INSULIN AND DEXAMETHASONE ON LIPOPROTEIN-LIPASE IN HUMAN ADIPOSE-TISSUE
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DOI：
10.1152/ajpendo.1992.262.5.e695
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发表时间：
1992-05-01
影响因子：
--
通讯作者：
FRIED, SK
中科院分区：
文献类型：
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作者：
APPEL, B;FRIED, SK
在器官培养中维持的人类脂肪组织碎片中检查了胰岛素和糖皮质激素调节脂蛋白脂肪酶（LPL）合成和降解的机制。 将组织碎片在添加或不添加胰岛素 (7 nM) 以及添加或不添加地塞米松 (30 nM)（一种合成糖皮质激素）的无血清培养基中培养 7 天。 LPL 活性对胰岛素和地塞米松的反应是在生理范围内的剂量下获得的。 在最大剂量下，胰岛素通过[S-35]蛋氨酸和[S-35]半胱氨酸脉冲标记和免疫沉淀确定的LPL合成速率（约5倍）特异性增加，从而增加肝素释放和总LPL活性（约7倍）。 与单独使用胰岛素相比，在存在胰岛素的情况下添加地塞米松可使肝素可释放活性和总 LPL 活性增加约 8 倍，但不会改变 LPL 合成速率。 脉冲追踪研究表明，与单独使用胰岛素相比，地塞米松加胰岛素的情况下 LPL 降解速度明显减慢。 这些数据表明，在人体脂肪组织中，胰岛素对于维持 LPL 合成速率至关重要，并且皮质醇可能通过抑制新合成的 LPL 降解，在翻译后水平调节人体脂肪组织 LPL 方面发挥关键作用。
The mechanisms by which insulin and glucocorticoids modulate lipoprotein lipase (LPL) synthesis and degradation were examined in human adipose tissue fragments maintained in organ culture. Tissue fragments were cultured for 7 days in serum-free medium supplemented with or without insulin (7 nM) and with or without dexamethasone (30 nM), a synthetic glucocorticoid. Responses of LPL activity to both insulin and dexamethasone were obtained at doses within the physiological range. At a maximal dose, insulin increased heparin-releasable and total LPL activity (approximately 7-fold) by specifically increasing the rate of LPL synthesis (approximately 5-fold) determined by pulse labeling with [S-35]methionine and [S-35]cysteine and immunoprecipitation. Dexamethasone added in the presence of insulin increased heparin-releasable and total LPL activity approximately 8-fold but did not alter rates of LPL synthesis compared with insulin alone. Pulse-chase studies showed that the rate of LPL degradation was markedly slowed in the presence of dexamethasone plus insulin compared with insulin alone. These data suggest that, in human adipose tissue, insulin is essential for maintaining rates of LPL synthesis and that cortisol may play a key role in regulating human adipose tissue LPL at the posttranslational level by inhibiting the degradation of newly synthesized LPL.