Eckel R H, Robbins R J
Proc Natl Acad Sci U S A. 1984 Dec;81(23):7604-7. doi: 10.1073/pnas.81.23.7604.
Lipoprotein lipase (LP lipase, triacylglycero-protein acylhydrolase EC 3.1.1.34) activity was found in four dissimilar brain regions (hypothalamus, cortex, cerebellum, and midbrain) of adult male rats. Progressive accumulation of LP lipase activity in cultured fetal rat hypothalamic cells was also observed, indicating de novo synthesis of the lipase. The brain LP lipase activity was serum-dependent and was inhibited by 1 M NaCl and by protamine sulfate. Kinetic analysis revealed an apparent Km of 0.79 mM very similar to that of rat adipose tissue LP lipase. That the lipase was functioning in the cultured brain cells was indicated by uptake and incorporation of radioactivity from tri[( 1-14C]oleoyl)glycerol into cellular triacylglycerols, and into more polar lipids, such as phosphatidylcholine. Furthermore, brain LP lipase activity in adult rats was decreased in all four regions examined, most significantly in the hypothalamus, after 72 hr of food deprivation. Thus, authentic LP lipase is present in adult rat brain and can be synthesized by isolated brain cells in vitro. LP lipase also mediates the uptake of triacylglycerol fatty acids and their subsequent incorporation into cellular lipids of cultured brain cells. Decreased brain LP lipase activity after fasting suggests that this enzyme may be regulated by metabolic or nutritional factors. Because the largest changes in LP lipase activity in response to food deprivation occurred in the hypothalamus, the enzyme may have a role in hypothalamic control of food intake or in body-weight regulation.
在成年雄性大鼠的四个不同脑区（下丘脑、皮层、小脑和中脑）中发现了脂蛋白脂肪酶（LP脂肪酶，三酰甘油蛋白酰基水解酶，EC 3.1.1.34）活性。在培养的胎鼠下丘脑细胞中也观察到LP脂肪酶活性的逐步积累，表明该脂肪酶是从头合成的。脑LP脂肪酶活性依赖于血清，并受到1 M氯化钠和硫酸鱼精蛋白的抑制。动力学分析显示，其表观Km为0.79 mM，与大鼠脂肪组织LP脂肪酶非常相似。三[（1-14C）油酰基]甘油中的放射性被摄取并掺入细胞三酰甘油以及更具极性的脂质（如磷脂酰胆碱）中，这表明该脂肪酶在培养的脑细胞中发挥作用。此外，禁食72小时后，成年大鼠所有四个检测脑区的脑LP脂肪酶活性均降低，在下丘脑中最为显著。因此，成年大鼠脑中存在真正的LP脂肪酶，并且离体脑细胞在体外可以合成该酶。LP脂肪酶还介导三酰甘油脂肪酸的摄取及其随后掺入培养脑细胞的细胞脂质中。禁食后脑LP脂肪酶活性降低表明该酶可能受代谢或营养因素的调节。由于禁食后LP脂肪酶活性变化最大的部位在下丘脑，该酶可能在下丘脑对食物摄入的控制或体重调节中起作用。
