Accelerated fat absorption in intestinal alkaline phosphatase knockout mice
Accelerated fat absorption in intestinal alkaline phosphatase knockout mice
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DOI：
10.1128/mcb.23.21.7525-7530.2003
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发表时间：
2003-11-01
影响因子：
5.3
通讯作者：
Millán, JL
中科院分区：
文献类型：
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作者：
Narisawa, S;Huang, L;Millán, JL
肠碱性磷酸酶（IAP）是AP基因家族中最古老的组织特异性成员。几项研究表明IAP具有吸收功能，但缺乏这种效果的体内数据。我们灭活了胚胎干细胞中的小鼠IAP基因，并产生了无效突变的纯合子小鼠。在正常实验室条件下，小鼠的肉眼和组织学检查正常且具有生育能力，与野生型对照组无差异。然而，当长期保持高脂肪饮食时，IAP缺陷小鼠的体重增加速度比对照组动物快。组织学检查显示，与野生型小鼠相比，IAP缺陷小鼠的脂肪滴通过肠上皮的运输加速，血清甘油三酯水平升高。我们的研究表明，IAP参与调节脂肪吸收的限速步骤。
Intestinal alkaline phosphatase (IAP) is the most ancestral of the tissue-specific members of the AP gene family. Several studies have suggested an absorptive function for IAP, but in vivo data to this effect have been lacking. We inactivated the mouse IAP gene in embryo-derived stem cells and generated mice homozygous for the null mutation. The mice were macroscopically and histologically normal and fertile and showed no difference from the wild-type controls under normal laboratory conditions. However, when maintained long-term on a high-fat diet, the IAP-deficient mice showed faster body weight gain than did control animals. Histological examination revealed an accelerated transport of fat droplets through the intestinal epithelium and elevation of serum triglyceride levels in the IAP-deficient mice compared to wild-type mice. Our study suggests that IAP participates in a rate-limiting step regulating fat absorption.