Ilundain A, Naftalin R J
Biochim Biophys Acta. 1981 Jun 22;644(2):316-22. doi: 10.1016/0005-2736(81)90389-8.
(1) The uptake and bidirectional fluxes of 1-alpha-methyl D-glucoside were studied in isolated rabbit colonic mucosa. (2) The uptake of alpha-methyl D-glucoside was linear over the first 30 min and reached maximum after 1 h; was a saturable function of sugar concentration and was Na+-dependent. (3) An increase in sugar uptake across the mucosal border and net transepithelial sugar flux across sheets of colon was observed in the presence of 10(-4) M amiloride. (4) Phlorizin (10(-4) M) inhibited sugar uptake into the tissue water and abolished net sugar flux. Amiloride-stimulated sugar uptake was also abolished by 10(-4) M phlorizin. (5) Ouabain (10(-4) M) prevented the effect of amiloride on sugar uptake and inhibited sugar uptake into the tissue. (6) These results corroborate the findings of Henriques de Jesus et al. (Henriques de Jesus, C., Da Gracia Emilio, M. and Santos, M.A. Gastroenterol. Clin. Biol. 3, 172-173) who found a sugar-dependent increase in short-circuit current in colonic mucosa exposed to amiloride.
(1)在离体兔结肠黏膜中研究了1-α-甲基-D-葡萄糖苷的摄取及双向通量。(2)α-甲基-D-葡萄糖苷的摄取在最初30分钟呈线性,1小时后达到最大值;是糖浓度的饱和函数且依赖于钠离子。(3)在存在10⁻⁴ M氨氯吡咪的情况下,观察到跨黏膜边界的糖摄取增加以及跨结肠片的净跨上皮糖通量增加。(4)根皮苷(10⁻⁴ M)抑制糖摄取进入组织液并消除净糖通量。10⁻⁴ M根皮苷也消除了氨氯吡咪刺激的糖摄取。(5)哇巴因(10⁻⁴ M)阻止了氨氯吡咪对糖摄取的作用并抑制糖摄取进入组织。(6)这些结果证实了恩里克斯·德·赫苏斯等人(恩里克斯·德·赫苏斯,C.,达·格拉西亚·埃米利奥,M.和桑托斯,M.A.《胃肠病学与临床生物学》3,172 - 173)的发现,他们发现暴露于氨氯吡咪的结肠黏膜中短路电流有糖依赖性增加。