Tan M H
Horm Metab Res. 1985 Nov;17(11):580-2. doi: 10.1055/s-2007-1013611.
The glucocorticoid-induced hypertriglyceridemia in uremic rats is partly due to defective removal of triglyceride (Tg)-rich lipoproteins. To determine whether this was due to decreased lipoprotein lipase (LPL), the key enzyme involved in the hydrolysis of Tg-rich lipoproteins, the LPL activity in soleus, heart and adipose tissue and the triglyceride secretion rates (TgSR) of uremic rats treated with Triamcinolone or placebo were studied. Sprague-Dawley rats were made uremic by a 2-stage 5/6 nephrectomy and studied three weeks later. During the 3rd week, one group was treated with a five day course of Triamcinolone (0.5 mg/kg body weight i.m.) and the other given an equal volume of saline. Triamcinolone aggravated the hypertriglyceridemia in uremic rats. This was associated with an increase in soleus and heart LPL with no change in adipose tissue LPL. The TgSR was also increased in the Triamcinolone-treated rats. These data suggest that decreased LPL activity is not the cause of hypertriglyceridemia in these rats.
糖皮质激素诱导的尿毒症大鼠高甘油三酯血症部分归因于富含甘油三酯（Tg）的脂蛋白清除缺陷。为了确定这是否是由于脂蛋白脂肪酶（LPL）减少所致，LPL是参与富含Tg的脂蛋白水解的关键酶，研究了用曲安西龙或安慰剂治疗的尿毒症大鼠比目鱼肌、心脏和脂肪组织中的LPL活性以及甘油三酯分泌率（TgSR）。通过两阶段5/6肾切除术使Sprague-Dawley大鼠患尿毒症，并在三周后进行研究。在第3周期间，一组接受为期五天的曲安西龙疗程（0.5mg/kg体重，肌肉注射），另一组给予等量的生理盐水。曲安西龙加重了尿毒症大鼠的高甘油三酯血症。这与比目鱼肌和心脏LPL增加有关，而脂肪组织LPL无变化。曲安西龙治疗的大鼠的TgSR也增加。这些数据表明，LPL活性降低不是这些大鼠高甘油三酯血症的原因。
