Carneheim C, Nedergaard J, Cannon B
Am J Physiol. 1984 Apr;246(4 Pt 1):E327-33. doi: 10.1152/ajpendo.1984.246.4.E327.
Lipoprotein lipase activity in adult rats was investigated in animals subjected to cold and to different hormonal treatments. In contrast to changes in tissue wet weight and total protein content, which showed a lag time of about 1 day, lipoprotein lipase activity was markedly (fourfold) increased after only 4 h in the cold. Total lipoprotein lipase activity reached a plateau already after 1-3 days, whereas wet weight and protein content did not plateau until 3 wk. Neither insulin nor glucose injections could mimic the cold-induced increase in lipoprotein lipase activity seen after 4 h. However, the effect of norepinephrine injections was identical to the effect of cold. The beta-agonist isoprenaline was as effective as norepinephrine, whereas the alpha-agonist phenylephrine had no effect. The beta-antagonist propranolol inhibited the cold-induced increase in lipoprotein lipase activity. It is concluded that, in contrast to white adipose tissue, brown adipose tissue lipoprotein lipase is stimulated in vivo by a beta-adrenergic mechanism and that it is this beta-adrenergic mechanism that is responsible for the rapid recruitment of lipoprotein lipase during cold exposure.
在成年大鼠中,对经受寒冷及不同激素处理的动物的脂蛋白脂肪酶活性进行了研究。与组织湿重和总蛋白含量的变化不同,后者显示出约1天的滞后时间,脂蛋白脂肪酶活性在寒冷环境中仅4小时后就显著增加(增至四倍)。总脂蛋白脂肪酶活性在1 - 3天后就达到了平台期,而湿重和蛋白含量直到3周后才达到平台期。胰岛素和葡萄糖注射均无法模拟在4小时后观察到的寒冷诱导的脂蛋白脂肪酶活性增加。然而,去甲肾上腺素注射的效果与寒冷的效果相同。β - 激动剂异丙肾上腺素与去甲肾上腺素效果相同,而α - 激动剂去氧肾上腺素则无作用。β - 拮抗剂普萘洛尔抑制了寒冷诱导的脂蛋白脂肪酶活性增加。得出的结论是,与白色脂肪组织不同,棕色脂肪组织脂蛋白脂肪酶在体内受β - 肾上腺素能机制刺激,且正是这种β - 肾上腺素能机制导致在寒冷暴露期间脂蛋白脂肪酶的快速募集。