Involvement of Intracellular Signaling in the IL‐1β Inhibitory Effect on Fructose Intestinal Absorption. Issue 4 (April 2015)

• Record Type: Journal Article
• Authors: Rodríguez‐Yoldi, María J.; Gascón, Sonia; Barranquero, Cristina; García‐Barrios, Alberto; Osada, Jesús
• Is Part Of: Journal of cellular physiology. Volume 230:Issue 4(2015:Apr.)
• Page Start: 896
• Page End: 902
• Publication Date: 2015-04
• Subjects: Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.24820
• Languages: English
• ISSNs: 0021-9541

Abstract

<abstract abstract-type="main" xml:lang="en"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="jcp24820-sec-0001" sec-type="section"> <p>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‐1β (IL‐1β) 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‐1β on <sc>D</sc>‐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‐1β treated rabbits. In addition, the activation of PI3K abolished the IL‐1β effect. Likewise, these results were confirmed in Caco‐2 cells. In addition, p‐PI3K expression was increased by IL‐1β‐treatment whereas the expression of p‐PKCα was not significantly affected. In summary, the results suggest that IL‐1β could regulate the activation of pPKCα 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.</p> </sec> </abstract>