Display options
Cite
Helliwell PA, Richardson M, Affleck J, et al. Stimulation of fructose transport across the intestinal brush-border membrane by PMA is mediated by GLUT2 and dynamically regulated by protein kinase C. Biochem J. 2000;350:149-54
Helliwell, P. A., Richardson, M., Affleck, J., & Kellett, G. L. (2000). Stimulation of fructose transport across the intestinal brush-border membrane by PMA is mediated by GLUT2 and dynamically regulated by protein kinase C. The Biochemical journal, 350149-54.
Helliwell, P A, et al. "Stimulation of fructose transport across the intestinal brush-border membrane by PMA is mediated by GLUT2 and dynamically regulated by protein kinase C." The Biochemical journal vol. 350 (2000): 149-54.
Helliwell PA, Richardson M, Affleck J, Kellett GL. Stimulation of fructose transport across the intestinal brush-border membrane by PMA is mediated by GLUT2 and dynamically regulated by protein kinase C. Biochem J. 2000 Aug 15;350:149-54. PMID: 10926838; PMCID: PMC1221236.
Copy Download .nbib Format: NLM
Share it on

Biochem J. 2000 Aug 15;350:149-54.

Stimulation of fructose transport across the intestinal brush-border membrane by PMA is mediated by GLUT2 and dynamically regulated by protein kinase C.

The Biochemical journal

P A Helliwell, M Richardson, J Affleck, G L Kellett

Affiliations

  1. Department of Biology, University of York, PO Box 373, York YO10 5YW, U.K.

PMID: 10926838 PMCID: PMC1221236

Abstract

Perfusion of rat jejunum in vitro with PMA increased fructose transport by 70% compared with control values and was blocked by the protein kinase C (PKC) inhibitor chelerythrine. The brush-border membrane contained both the fructose transporters GLUT5 and GLUT2; the presence of the latter was confirmed by luminal biotinylation. PMA increased the GLUT2 level 4-fold within minutes, so that the level was comparable with that of the basolateral membrane, but had no effect on GLUT5 level. GLUT2 was functional, accessible to luminal fructose and could be inhibited selectively by phloretin to permit determination of GLUT2- and GLUT5-mediated transport components. The 4-fold increase in GLUT2 level induced by PMA was matched by a 4-fold increase in GLUT2-mediated transport: there was a compensatory fall in the GLUT5-mediated rate. The pattern of dynamic trafficking was seen only for GLUT2, not GLUT5 or SGLT1, implying that GLUT2 trafficks to the brush-border membrane by a different pathway. Trafficking of GLUT2 to the brush-border membrane correlated with activation of PKC betaII, implying that this isoenzyme is likely to control trafficking. Since PKC is activated by endogenous hormones, GLUT2 levels in vivo are 3-4-fold those in vitro; moreover, because PKC is inactivated as soon as intestine is excised, GLUT2 is lost from the brush-border within minutes in vitro. It is therefore difficult to detect GLUT2 in most in vitro preparations and its role in intestinal sugar absorption across the brush-border membrane has accordingly been overlooked.

References

  1. Proc Natl Acad Sci U S A. 1990 Dec;87(24):9893-7 - PubMed
  2. Am J Physiol. 1990 Dec;259(6 Pt 1):C279-85 - PubMed
  3. Am J Physiol. 1992 Mar;262(3 Pt 1):C795-800 - PubMed
  4. Gastroenterology. 1993 Oct;105(4):1050-6 - PubMed
  5. Exp Physiol. 1994 Mar;79(2):203-14 - PubMed
  6. J Cell Biol. 1994 Aug;126(3):747-63 - PubMed
  7. J Physiol. 1994 Jul 15;478 ( Pt 2):187-93 - PubMed
  8. Pflugers Arch. 1996 Jun;432(2):192-201 - PubMed
  9. Biochem J. 1998 Jun 1;332 ( Pt 2):281-92 - PubMed
  10. Biochem J. 2000 Aug 15;350 Pt 1:155-62 - PubMed
  11. Biochem J. 2000 Aug 15;350 Pt 1:163-9 - PubMed
  12. Biochim Biophys Acta. 1974 Oct 29;367(2):247-54 - PubMed
  13. Biochem J. 1984 May 1;219(3):1027-35 - PubMed
  14. Gut. 1988 Aug;29(8):1064-9 - PubMed
  15. Biochim Biophys Acta. 1989 Mar 13;979(3):311-5 - PubMed
  16. Comp Biochem Physiol A Comp Physiol. 1991;100(1):175-82 - PubMed

Substances

MeSH terms

Publication Types