Csáky T Z, Fischer E
Biochim Biophys Acta. 1984 May 30;772(3):259-63. doi: 10.1016/0005-2736(84)90142-1.
It was observed previously (Cs aky , T.Z. and Fischer, E. (1981) Diabetes 30, 568-574), that sustained hyperglycemia enhances the intestinal transport of aldohexoses ; on the other hand, hyperfructosemia affects primarily the transport of fructose. The present study examines in detail the hyperketosemia -induced intestinal ketose transport. Intravenously infused 3-O- methylfructose produces marked 3-O- methylfructosemia without concomitant hyperglycemia; in such animals the intestinal transport of both fructose and 3-O- methylfructose increased. The hyperketosemia -induced increased ketose transport was inhibited by phloretin but only if placed on the serosal compartment. Phlorizin affects neither the basal nor the induced intestinal ketohexose transport. The enhancement of the intestinal ketohexose transport is not sodium-dependent and is not inhibited by ouabain.
先前已有观察（察斯基，T.Z.和菲舍尔，E.（1981年），《糖尿病》30卷，568 - 574页）表明，持续性高血糖会增强肠道对己醛糖的转运；另一方面，高果糖血症主要影响果糖的转运。本研究详细考察了高酮血症诱导的肠道酮糖转运。静脉注射3 - O - 甲基果糖会产生显著的3 - O - 甲基果糖血症，而无伴随的高血糖；在这类动物中，果糖和3 - O - 甲基果糖的肠道转运均增加。高酮血症诱导的酮糖转运增加被根皮素抑制，但前提是将其置于浆膜腔室。根皮苷对基础的或诱导的肠道酮己糖转运均无影响。肠道酮己糖转运的增强不依赖于钠，且不受哇巴因抑制。
