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The administration of lipopolysaccharide, in vivo, induces alteration in L-leucine intestinal absorption.

机译:体内脂多糖的施用诱导L-亮氨酸肠吸收的改变。

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The objective of the present study was to determine the alterations in L-leucine intestinal uptake by intravenous administration of Lipopolysaccharide (LPS), which is a constituent of gram negative bacterial, causative agent of sepsis. The amino acid absorption in LPS treated rabbits was reduced compared to the control animals. The LPS effect on the amino acid uptake was due to an inhibition of the Na+-dependent system of transport, through both reduction of the apparent capacity transport (Vmax) and diminution of the Na+/K-ATPase activity. The results have also shown that the LPS decreases the mucosal to serosal transepithelial flux and the transport across brush border membrane vesicles of L-leucine. The study of possible intracellular mechanisms implicated in the LPS effect, showed that the second messengers calcium, protein kinase C and c-AMP did not play any role in this effect. However, the absence of ion chloride in the incubation medium removes the LPS inhibition and the intracellular tissue water was affected by the LPS treatment. Therefore, the inhibition in the L-leucine intestinal absorption, by intravenous administration of LPS, could be mainly produced by the secretagogue action of this endotoxin on the gut.
机译:本研究的目的是通过静脉内施用脂多糖(LPS)来确定L-亮氨酸肠道摄取的变化,脂多糖是革兰氏阴性细菌,败血症的致病因子。与对照动物相比,经LPS处理的兔子的氨基酸吸收减少。 LPS对氨基酸摄取的影响是由于通过减少表观容量运输(Vmax)和减少Na + / K-ATPase活性而抑制了Na +依赖性运输系统。结果还表明,LPS降低了粘膜到浆膜的上皮通量以及L-亮氨酸的刷状缘膜囊泡的转运。对可能与LPS作用有关的细胞内机制的研究表明,第二信使钙,蛋白激酶C和c-AMP在该作用中没有任何作用。然而,温育培养基中不存在离子氯化物消除了LPS抑制作用,并且LPS处理会影响细胞内组织水。因此,静脉内施用LPS对L-亮氨酸肠吸收的抑​​制作用主要是由这种内毒素对肠道的促分泌作用产生的。

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