Silverman M, Huang L
Am J Physiol. 1976 Oct;231(4):1024-32. doi: 10.1152/ajplegacy.1976.231.4.1024.
The multiple indicator-dilution technique in vivo and isolated brush-border membranes in vitro have been used to explore the mechanism of maleic acid-induced glucosuria in dog kidney. The interaction of D-glucose with the antiluminal membrane from the peritubular fluid surface is unaltered. It is demonstrated that alpha-methyl-D-glucoside (alpha MG) enters and exits from the proximal tubular cell only across the brush-border membrane. Then using alphaMG as a reference indicator, it is shown that maleic acid does not cause complete inhibition of D-glucose interaction with the antiluminal membrane from the cytoplasmic surface. The binding of [3H]phlorizin both in vivo and in vitro is not affected by prior administration of maleic acid, indicating that D-glucose interaction with the outside surface of the brush border is also not affected by maleic acid. The data are therefore consistent with the concept that maleic acid-induced glucosuria is due either to i) partial inhibition of D-glucose movement from cytoplasm across the antiluminal membrane into the blood, ii) stimulated movement back across the brush-border membrane into urine, or iii) a combination of the two effects.
体内多指示剂稀释技术和体外分离的刷状缘膜已被用于探究顺丁烯二酸诱导犬肾糖尿的机制。D-葡萄糖与肾小管周围液体表面的抗腔面膜之间的相互作用未改变。结果表明，α-甲基-D-葡萄糖苷（αMG）仅通过刷状缘膜进出近端肾小管细胞。然后以αMG作为参考指示剂，结果显示顺丁烯二酸不会完全抑制D-葡萄糖与细胞质表面抗腔面膜的相互作用。体内和体外[3H]根皮苷的结合不受预先给予顺丁烯二酸的影响，这表明D-葡萄糖与刷状缘外表面的相互作用也不受顺丁烯二酸的影响。因此，这些数据与以下概念一致，即顺丁烯二酸诱导的糖尿是由于：i）D-葡萄糖从细胞质穿过抗腔面膜进入血液的过程受到部分抑制；ii）刺激其穿过刷状缘膜返回尿液；或iii）这两种效应的组合。
