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经肠腔和血管灌注的大鼠肠道对锌的吸收动力学

Kinetics of zinc absorption by luminally and vascularly perfused rat intestine.

作者信息

Steel L, Cousins R J

出版信息

Am J Physiol. 1985 Jan;248(1 Pt 1):G46-53. doi: 10.1152/ajpgi.1985.248.1.G46.

DOI:10.1152/ajpgi.1985.248.1.G46
PMID:3966560
Abstract

Zinc absorption by intestines of rats fed either zinc-deficient or zinc-adequate diets was measured by simultaneous luminal and vascular perfusion. The rate of absorption increased steadily for the first 30-40 min of perfusion over the entire lumen zinc concentration range examined (8-234 microM). During the last 10 min of perfusion the absorption rate did not change appreciably with time (steady state), and absorption by intestines from the zinc-depleted rats showed evidence of both carrier-mediated (saturable) and nonmediated (nonsaturable) components. The former had a Km of 55 microM and a Jmax of 3.3 nmol X min-1. In contrast, the absorption rate during the last 10 min of the perfusion period was a sigmoidal function of the luminal zinc concentration with intestines from zinc-adequate rats. The cytosol 65Zn concentration increased proportionately with increased luminal 65Zn concentration but was significantly greater in intestines from zinc-depleted rats. Both high-molecular-weight species and metallothionein accounted for this increase in cytosolic 65Zn. An increase in the vascular bed zinc concentration increased the amount of zinc transferred to the mucosal cytosol but did not increase the amount transferred to the lumen. These results suggest a second mechanism of absorption may be induced during a dietary zinc depletion that is carrier mediated. Moreover, while zinc is transferred in the vascular-to-mucosal direction from the vascular supply, little actually enters the lumen.

摘要

通过同时进行肠腔和血管灌注,测量了喂食缺锌或锌充足日粮的大鼠肠道对锌的吸收情况。在所研究的整个肠腔锌浓度范围(8 - 234微摩尔)内,灌注的前30 - 40分钟,吸收速率稳步增加。在灌注的最后10分钟内,吸收速率随时间没有明显变化(稳态),缺锌大鼠肠道的吸收表现出载体介导(可饱和)和非介导(不可饱和)成分的证据。前者的米氏常数为55微摩尔,最大反应速率为3.3纳摩尔×分钟⁻¹。相比之下,对于锌充足大鼠的肠道,灌注期最后10分钟的吸收速率是肠腔锌浓度的S形函数。细胞质中⁶⁵锌的浓度随肠腔中⁶⁵锌浓度的增加而成比例增加,但在缺锌大鼠的肠道中显著更高。高分子量物质和金属硫蛋白都导致了细胞质中⁶⁵锌的这种增加。血管床锌浓度的增加增加了转移到粘膜细胞质中的锌量,但没有增加转移到肠腔中的锌量。这些结果表明,在饮食锌缺乏期间可能会诱导一种由载体介导的第二种吸收机制。此外,虽然锌从血管供应以血管到粘膜的方向转移,但实际上很少进入肠腔。

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