Intestinal gluconeogenesis and glucose transport according to body fuel availability in rats
Intestinal gluconeogenesis and glucose transport according to body fuel availability in rats
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DOI：
10.1113/jphysiol.2005.085217
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发表时间：
2005-07-15
影响因子：
5.5
通讯作者：
Oudart, H
中科院分区：
文献类型：
--
作者：
Habold, C;Foltzer-Jourdainne, C;Oudart, H
肠己糖的吸收和肠异生已经研究了两个不同的禁食阶段后的再喂养：一个长时间的蛋白质节约期间，能量消耗来自脂质氧化（第二阶段），和后期的特点是血浆皮质酮触发蛋白catenin（第三阶段）的上升。这种身体燃料使用的转换，导致身体储备和代谢前体的变化，可以调节肠道代谢和葡萄糖转运。测定钠-葡萄糖协同转运蛋白SGLT 1、GLUT 5和GLUT 2的基因和蛋白质水平以及细胞定位，以及关键的促凋亡酶磷酸烯醇式丙酮酸羧激酶（PEPCK）和葡萄糖-6-磷酸酶（Glc 6-phosphatase，Glc 6-phosphatase）的基因和蛋白质水平以及细胞定位。同时测定PEPCK和Glc 6 β活性。在III期禁食大鼠中，SGLT 1上调，肠道葡萄糖摄取率高于II期禁食和进食大鼠。PEPCK和Glc 6 β mRNA、蛋白水平和活性在III期也增加。GLUT 5和GLUT 2在整个禁食过程中下调，但在重新进食后增加，GLUT 2被招募到顶端膜。在III期期间SGLT 1表达的增加可能允许在食物可用时尽快吸收低浓度的葡萄糖。此外，由于禁食而增加的上皮渗透性可诱导葡萄糖的细胞旁运动。在禁食期间肠道GLUT 2不存在的情况下，Glc 6 β可能参与葡萄糖通过膜运输释放到血流中。最后，再喂养触发GLUT 2和GLUT 5的合成和GLUT 2的顶端募集，以吸收更大量的己糖。
Intestinal hexose absorption and gluconeogenesis have been studied in relation to refeeding after two different fasting phases: a long period of protein sparing during which energy expenditure is derived from lipid oxidation (phase II), and a later phase characterized by a rise in plasma corticosterone triggering protein catabolism (phase III). Such a switch in body fuel uses, leading to changes in body reserves and gluconeogenic precursors, could modulate intestinal gluconeogenesis and glucose transport. The gene and protein levels, and the cellular localization of the sodium-glucose cotransporter SGLT1, and of GLUT5 and GLUT2, as well as that of the key gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (Glc6Pase) were measured. PEPCK and Glc6Pase activities were also determined. In phase III fasted rats, SGLT1 was up-regulated and intestinal glucose uptake rates were higher than in phase II fasted and fed rats. PEPCK and Glc6Pase mRNA, protein levels and activities also increased in phase III. GLUT5 and GLUT2 were down-regulated throughout the fast, but increased after refeeding, with GLUT2 recruited to the apical membrane. The increase in SGLT1 expression during phase III may allow glucose absorption at low concentrations as soon as food is available. Furthermore, an increased epithelial permeability due to fasting may induce a paracellular movement of glucose. In the absence of intestinal GLUT2 during fasting, Glc6Pase could be involved in glucose release to the bloodstream via membrane trafficking. Finally, refeeding triggered GLUT2 and GLUT5 synthesis and apical recruitment of GLUT2, to absorb larger amounts of hexoses.