Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

Inflamm Res. 2003 Apr;52(4):177-84. doi: 10.1007/s000110300069.

Abstract

Objective: To investigate alterations in the transport of D-fructose across the rabbit jejunum when the gut is exposed in vitro to lipopolysaccharide (LPS), an endotoxin causative agent of sepsis.

Materials and methods: D-fructose intestinal transport was assesed employing three techniques: sugar uptake measurements in rings of everted jejunum (micromol/D-fructose/ml cell water), transepithelial flux measurements in Ussing-type chambers (micromol D-fructose/cm2/h) and transport assays in preparation of brush border membrane vesicles (pmoles D-fructose/mg protein). Samples were taken from the bathing solution and from the extracts of the tissue for radioactivity counting.

Results: Adding LPS (3 microg/ml) to tissue decreased the uptake and mucosal to serosal flux of 5 mM D-fructose across the enterocyte. LPS did not modify sugar uptake across brush border membrane vesicles. The inhibitory effect of LPS was suppressed by W-13 (5 x 10(-6) M), a Ca-calmodulin antagonist, and staurosporine (10(-7) and 10(-6) M) and GF-109203X (10(-6) M) a nonselective and selective protein kinase C (PKC) inhibitor respectively. Tumor Necrosis Factor (TNF-alpha), an immunoregulatory cytokine involved in septic responses occurring during bacterial infection at concentrations 3 x 10(-4) to 3 microg/ml, did not affect the sugar transport.

Conclusions: LPS can inhibit the intestinal uptake of D-fructose across the rabbit jejunum in vitro by intracellular processes related to PKC and calmodulin protein.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Body Water / metabolism
  • Calmodulin / metabolism
  • Dose-Response Relationship, Drug
  • Endotoxins / toxicity
  • Epithelium / drug effects
  • Epithelium / metabolism
  • Fructose / metabolism*
  • In Vitro Techniques
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism
  • Jejunum / metabolism*
  • Lipopolysaccharides / pharmacology*
  • Male
  • Microvilli / drug effects
  • Microvilli / metabolism
  • Protein Kinase C / metabolism
  • Rabbits
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Calmodulin
  • Endotoxins
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Fructose
  • endotoxin, Escherichia coli
  • Protein Kinase C