In vitro activation of the enzymic activity of hepatic lipase by apoA‐II
In vitro activation of the enzymic activity of hepatic lipase by apoA‐II
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apoA-II 体外激活肝脂肪酶的酶活性
DOI：
10.1016/0014-5793(81)80405-x
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发表时间：
1981
期刊：
影响因子：
3.5
通讯作者：
H. Brewer
中科院分区：
文献类型：
--
作者：
C. Jahn;J. C. Osborne;E. Schaefer;H. Brewer
人肝素后血浆含有两种主要脂肪酶活性，即脂蛋白脂肪酶（LPL）和肝脂肪酶（HL）[1-3]。LPL由apoC-II [4，5]和aport（β 2糖蛋白I）[6]激活。I型高脂蛋白血症与LPL酶活性缺乏相关[7]。apoC-1 I的缺乏也会导致I型高脂蛋白血症[8]，因此，LPL和apoC-11被认为在调节人体内富含谷氨酰胺脂蛋白的代谢方面具有重要意义。在患有肝病和肾衰竭的患者中，肝素后人血浆中的HL活性降低[9- 11]。据报道，HL酶活性与高密度脂蛋白（HDL，d= 1.063-1.21 g/ml [12]）以及HDL 2（d--1.063-1.125 g/ml）的浓度呈负相关，并表明HL可能在HDL 2的催化作用中发挥作用[13]。据报道，HL酶活性受到载脂蛋白CI、C-II和C-III的抑制，并受到高浓度NaCl和血清的增加[14]。在初步研究中，我们还观察到人血浆可激活HL酶活性。本研究的目的是进一步确定血浆中负责这种激活的组分。我们的调查结果表明，在研究的条件下，apoA-II，人HDL的蛋白质成分激活HL。
Human post-heparin plasma contains two major lipase activities designated lipoprotein lipase (LPL) and hepatic lipase (HL)[1-3]. LPL is activated by apoC-II [4, 5] and aport (/32 glycoprotein I)[6]. Type I hyperlipoproteinemia is associated with a deficiency in the enzymic activity of LPL [7]. A deficiency in apoC-1I also results in type I hyperlipoproteinemia [8] and LPL and apoC-I1 have therefore been proposed to be of major importance in modulating the catabolism of triglyceride-rich lipoproteins in man. The function, natural substrate and regulation of the enzymic activity of ilL have been less well defined. HL activity in human post-heparin plasma is decreased in patients with liver disease and renal failure [9-1 1]. An inverse correlation between HL enzymic activity and the concentration of high density lipoproteins (HDL, d= 1.063-1.21 g/ml [12]) as well as HDL2 (d--1.063-1.125 g/ml) has been reported and it has been suggested that HL may play a role in the catabolism of HDL2 [13]. HL enzymic activity has been reported to be inhibited by apolipoproteins CI, C-II and C-III, and increased by high concentrations of NaC1 and serum [14]. In initial studies we have also observed that human plasma activates HL enzymic activity. It was the purpose of this study to further define the component within plasma which is responsible for this activation. The results of our investigations indicate that under the conditions studied, apoA-II, a protein constituent of human HDL activates HL.