title: Inhibitory effect of IL-1β on galactose intestinal absorption in rabbits.
abstract: OBJECTIVE
  Recent studies from our laboratory have shown that nitric oxide is involved in the IL-1β-induced inhibition of D-fructose intestinal transport in rabbits. The aim of this work was to further the studies of IL-1β effect on D-galactose absorption in a septic state induced by intravenous administration of this cytokine.
  
  
  METHODS
  Galactose intestinal absorption was assessed employing three techniques: sugar uptake in jejunum everted rings, transepithelial flux in Ussing-type chambers and uptake assays in brush border membrane vesicles. The level of the Na(+)/D-glucose cotransporter (SGLT1) expression was analyzed by Western blot.
  
  
  RESULTS
  In sepsis condition the body temperature was increased and studies on cellular intestinal integrity have not shown modifications in the brush border membrane. However, D-galactose absorption across mucosa of jejunum was diminished in IL-1β treated rabbits. The levels of SGLT-1 were no significantly different in both animal groups (control and IL-1β treated), indicating that the cytokine could induce a reduction in the SGLT-1 functionality. The inhibition was significantly reversed by the activation of several PKC, PKA, MAPKs and nuclear factor (NF)-ĸB inhibitors administered 15 min before the IL-1β.
  
  
  CONCLUSIONS
  The inhibitory effect of IL-1β on D-galactose absorption across mucosal side of enterocyte could be mediated by the activation of several kinases and nuclear factor (NF)-ĸB.
authors: Unidad de Fisiología, Departamento de Farmacología y Fisiología, Facultad de Veterinaria, Universidad de Zaragoza, Zaragoza, Spain.
authors: Carmen
authors: C
authors: Viñuales
authors: Sonia
authors: S
authors: Gascón
authors: Cristina
authors: C
authors: Barranquero
authors: Jesús
authors: J
authors: Osada
authors: Ma Jesús
authors: MJ
authors: Rodríguez-Yoldi
mesh_terms: D000818:Animals; D002867:Chromones / Q000494:pharmacology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors; D005690:Galactose / Q000378:metabolism*; D019833:Genistein / Q000494:pharmacology; D066298:In Vitro Techniques; D007211:Indoles / Q000494:pharmacology; D053583:Interleukin-1beta / Q000494:pharmacology / Q000502:physiology*; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000378:metabolism; D007583:Jejunum / Q000378:metabolism / Q000473:pathology; D008297:Male; D008301:Maleimides / Q000494:pharmacology; D008871:Microvilli / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D009025:Morpholines / Q000494:pharmacology; D016328:NF-kappa B / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011817:Rabbits; D018805:Sepsis / Q000378:metabolism; D051269:Sodium-Glucose Transporter 1 / Q000378:metabolism
chemical_list: D002867:Chromones; D007211:Indoles; D053583:Interleukin-1beta; D008301:Maleimides; D009025:Morpholines; D016328:NF-kappa B; D000081082:Phosphoinositide-3 Kinase Inhibitors; D047428:Protein Kinase Inhibitors; D051269:Sodium-Glucose Transporter 1; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D019833:Genistein; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D020928:Mitogen-Activated Protein Kinases; C070515:bisindolylmaleimide I; D005690:Galactose