Involvement of Intracellular Signaling in the IL-1[beta] Inhibitory Effect on Fructose Intestinal Absorption
A variety of bacteria and their excreted/secreted products having direct effects on epithelial ion transport and permeability and the release of cytokines during bacterial infection may impact directly on epithelial function. Interleukin-1[beta] (IL-1[beta]) is a pleiotropic cytokine that affects th...
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Published in | Journal of cellular physiology Vol. 230; no. 4; p. 896 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc
01.04.2015
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Subjects | |
Online Access | Get full text |
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Summary: | A variety of bacteria and their excreted/secreted products having direct effects on epithelial ion transport and permeability and the release of cytokines during bacterial infection may impact directly on epithelial function. Interleukin-1[beta] (IL-1[beta]) is a pleiotropic cytokine that affects the intestinal absorption of nutrients. The aim of this work was to study the intracellular signaling pathways involved in the inhibitory effect of IL-1[beta] on D-fructose intestinal transport in rabbit jejunum and Caco-2 cells. The results show that the cytokine inhibitory effect was completely reversed in presence of proteasome or PKC selective inhibitors in IL-1[beta] treated rabbits. In addition, the activation of PI3K abolished the IL-1[beta] effect. Likewise, these results were confirmed in Caco-2 cells. In addition, p-PI3K expression was increased by IL-1[beta]-treatment whereas the expression of p-PKC[alpha] was not significantly affected. In summary, the results suggest that IL-1[beta] could regulate the activation of pPKC[alpha] 73, pPI3K 55, and NF-kB proteins. These events could exert an inhibitory effect on fructose intestinal absorption by a modification of GLUT5 insertion to brush-border membrane and/or the functional transporter activity. This effect is independent of hormonal milieu and nervous stimuli. J. Cell. Physiol. 230: 896-902, 2015. © 2014 Wiley Periodicals, Inc. |
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ISSN: | 0021-9541 1097-4652 |
DOI: | 10.1002/jcp.24820 |