Neafsey P J, Schwartz R
J Nutr. 1977 Jun;107(6):1061-7. doi: 10.1093/jn/107.6.1061.
Rats depleted of magnesium for 13 days were killed after 18 to 20 hours of fasting or 2 hours after consumption of a standard-sized meal. Serum and duodenal alkaline phosphatase (AP) were reduced in fasted magnesium depleted rats compared to pair-fed and ad libitum-fed controls. With refeeding, serum alkaline phosphatase levels rose significantly in all groups, but the levels in refed Mg deficient rats remained below serum levels of fasted control rats. Inhibition of AP activity with L-phenylalanine and urea suggested that the differences in AP levels of fasted and fed rats were mainly due to enzymes of intestinal origin. Intestinal AP levels increased after feeding in all groups, but were proportionately greatest in Mg depleted rats. The pattern of serum and duodenal AP in fed and fasted rats and the results of polyacrylamide disc gel electrophoresis (PADGE) in duodenal AP extracts suggest that Mg depletion alters the release of AP into the blood that normally occurs in response to feeding.
缺镁13天的大鼠在禁食18至20小时后或进食标准量餐食2小时后被处死。与成对喂食和自由进食的对照组相比，禁食的缺镁大鼠血清和十二指肠碱性磷酸酶（AP）降低。重新喂食后，所有组的血清碱性磷酸酶水平均显著升高，但重新喂食的缺镁大鼠的水平仍低于禁食对照大鼠的血清水平。用L-苯丙氨酸和尿素抑制AP活性表明，禁食和喂食大鼠AP水平的差异主要归因于肠道来源的酶。所有组喂食后肠道AP水平均升高，但缺镁大鼠升高幅度最大。喂食和禁食大鼠血清和十二指肠AP的模式以及十二指肠AP提取物的聚丙烯酰胺圆盘凝胶电泳（PADGE）结果表明，缺镁会改变正常情况下因进食而发生的AP释放到血液中的情况。
