Abad B, Mesonero J E, Salvador M T, Garcia-Herrera J, Rodriguez-Yoldi M J
Physiology Unit, Veterinary Faculty, University of Zaragoza, Spain.
Dig Dis Sci. 2001 May;46(5):1113-9. doi: 10.1023/a:1010782600380.
In the present study, we have investigated whether the lipopolysaccharide (LPS) endotoxin from Escherichia coli is able to alter the jejunal transport of L-leucine when the tissue is exposed to endotoxin. The results have shown that the LPS at 3 x 10(-5) microg/ml decreases the uptake of L-leucine into the enterocyte, as well as the mucosal to serosal flux of L-leucine. The secretagogue effect of LPS on the gut did not affect the inhibitory effect of LPS on the intestinal absorption of the amino acid. The endotoxin did not modify amino acid diffusion across the intestinal epithelium. However, from the mediated transport, only the Na+-dependent transport system was affected by LPS with a diminution of the transporter affinity (the apparent Km was increased). In addition, we found a reduction of the Na+, K+-ATPase activity, which could explain the L-leucine Na+-dependent transport inhibition.
在本研究中,我们调查了来自大肠杆菌的脂多糖(LPS)内毒素在组织暴露于内毒素时是否能够改变空肠对L-亮氨酸的转运。结果表明,3×10⁻⁵微克/毫升的LPS会降低L-亮氨酸进入肠细胞的摄取量,以及L-亮氨酸从黏膜到浆膜的通量。LPS对肠道的促分泌作用并未影响其对氨基酸肠道吸收的抑制作用。内毒素并未改变氨基酸跨肠上皮的扩散。然而,在介导转运方面,只有Na⁺依赖性转运系统受到LPS影响,转运体亲和力降低(表观Km增加)。此外,我们发现Na⁺,K⁺-ATP酶活性降低,这可以解释L-亮氨酸Na⁺依赖性转运受到抑制的原因。