Chu S W, Geyer R P, Walker W A
Biochim Biophys Acta. 1987 Jul 6;929(2):220-5. doi: 10.1016/0167-4889(87)90179-0.
The influence of phosphatidylinositol (PI) on intestinal alkaline phosphatase activity was studied in myo-inositol deficient gerbils. A reduction of membrane PI in intestinal mucosa to 30-40% of the control was produced by feeding female gerbils a myo-inositol-deficient diet containing coconut oil for 2 weeks. As expected, the animals developed typical intestinal lipodystrophy with abnormal fat accumulation. In the PI-depleted animal, intestinal alkaline phosphatase activity was reduced to 20-30% of the control group. The levels of both membranous and soluble enzymes in intestinal mucosa were affected, but there were no changes in liver, kidney and plasma levels. When the lipodystrophic gerbils were given dietary myo-inositol, the complete repletion of intestinal membrane PI to the control level occurred 36 h later, whereas membrane-bound alkaline phosphatase activity in intestine was not restored to the control level until 72 h later. Administration of cycloheximide or actinomycin D did not block this enzyme induction. Lymphatic output of triacylglycerol into the bloodstream was stimulated 10-fold at 18 h of myo-inositol repletion, but there was no parallel increase in the activity of alkaline phosphatase in plasma during this early phase of intestinal recovery. Thus, these data suggest a possible regulatory role of PI in the processing and/or turnover of alkaline phosphatase in vivo, but a negative role of alkaline phosphatase in lipid transport across gerbil intestine.
在肌醇缺乏的沙鼠中研究了磷脂酰肌醇（PI）对肠道碱性磷酸酶活性的影响。通过给雌性沙鼠喂食含椰子油的肌醇缺乏饮食2周，使肠道黏膜中的膜PI减少至对照水平的30 - 40%。正如预期的那样，这些动物出现了典型的肠道脂肪营养不良，伴有异常的脂肪堆积。在PI耗竭的动物中，肠道碱性磷酸酶活性降低至对照组的20 - 30%。肠道黏膜中膜结合型和可溶性酶的水平均受到影响，但肝脏、肾脏和血浆中的水平没有变化。当给脂肪营养不良的沙鼠喂食肌醇时，肠道膜PI在36小时后完全恢复到对照水平，而肠道中膜结合型碱性磷酸酶活性直到72小时后才恢复到对照水平。给予环己酰亚胺或放线菌素D并不能阻断这种酶的诱导。在补充肌醇18小时时，三酰甘油进入血液循环的淋巴输出量增加了10倍，但在肠道恢复的这个早期阶段，血浆中碱性磷酸酶的活性并没有相应增加。因此，这些数据表明PI在体内碱性磷酸酶的加工和/或周转中可能具有调节作用，但碱性磷酸酶在沙鼠肠道脂质转运中具有负面作用。
