Eliakim R, Mahmood A, Alpers D H
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.
Biochim Biophys Acta. 1991 Jan 10;1091(1):1-8. doi: 10.1016/0167-4889(91)90213-h.
We have reported the presence of intestinal alkaline phosphatase on particles with surfactant-like properties within enterocytes, on the luminal surface (light mucosal scrapings) and in the lumen of adult fat-fed rat intestines ((1989) J. Clin. Invest. 84, 1355). To test the physiological role of these particles, we compared the effect on particle secretion of a known inducer of luminal and serum alkaline phosphatase secretion (fat), with the effect of pharmacological stimulators (cholecystokinin and bethanecol). Fat induced a 2-3-fold increase in membrane-free phosphatase activity in serum, and in particle-bound alkaline phosphatase activity in proximal luminal washings and light mucosal scrapings, reaching a peak in both compartments 7 h after a corn oil feed. Bethanecol given subcutaneously induced a quantitatively similar increase in serum alkaline phosphatase activity and in particle-bound phosphatase activity in proximal light mucosal scrapings, reaching a peak 7.5 min after injection. Cholecystokinin also had a 2-3-fold stimulatory effect, 30 min after injection, on particle-bound phosphatase activity in proximal intestinal light mucosal scrapings and distal intestinal luminal washings. The increase in alkaline phosphatase activity in serum samples reached a peak 60 min after cholecystokinin injection. Thus, three independent stimuli increase both luminal and serum appearance of intestinal alkaline phosphatase. These data support the earlier findings that intestinal alkaline phosphatase secretion into the lumen is mediated by a secreted particle, further show that secretion into serum and lumen is coordinately regulated, and are consistent with the hypothesis that the rise in serum alkaline phosphatase activity could be related to extracellular release of the enzyme from the particles.
我们曾报道，在成年高脂喂养大鼠的肠细胞内具有表面活性剂样性质的颗粒上、管腔表面（轻度黏膜刮片）以及肠腔内存在肠碱性磷酸酶（(1989)《临床研究杂志》84, 1355）。为了测试这些颗粒的生理作用，我们比较了一种已知的管腔和血清碱性磷酸酶分泌诱导剂（脂肪）对颗粒分泌的影响，以及药理学刺激剂（胆囊收缩素和氨甲酰甲胆碱）的影响。脂肪使血清中无膜磷酸酶活性以及近端管腔冲洗液和轻度黏膜刮片中颗粒结合的碱性磷酸酶活性增加2 - 3倍，在给予玉米油饲料后7小时，两个部位均达到峰值。皮下注射氨甲酰甲胆碱使血清碱性磷酸酶活性以及近端轻度黏膜刮片中颗粒结合的磷酸酶活性在数量上有类似增加，注射后7.5分钟达到峰值。注射胆囊收缩素30分钟后，对近端肠轻度黏膜刮片和远端肠腔冲洗液中颗粒结合的磷酸酶活性也有2 - 3倍的刺激作用。胆囊收缩素注射后60分钟，血清样本中碱性磷酸酶活性增加达到峰值。因此，三种独立的刺激均增加了肠碱性磷酸酶在管腔和血清中的出现。这些数据支持了早期的研究结果，即肠碱性磷酸酶向管腔的分泌是由一种分泌颗粒介导的，进一步表明向血清和管腔的分泌受到协调调节，并且与血清碱性磷酸酶活性升高可能与该酶从颗粒的细胞外释放有关的假设一致。
