GLUT5
GLUT5 is a fructose transporter expressed on the apical border of enterocytes in the small intestine.[5] GLUT5 allows for fructose to be transported from the intestinal lumen into the enterocyte by facilitated diffusion due to fructose's high concentration in the intestinal lumen. GLUT5 is also expressed in skeletal muscle,[6] testis, kidney, fat tissue (adipocytes), and brain.[7]
Fructose malabsorption or Dietary Fructose Intolerance is a dietary disability of the small intestine, where the amount of fructose carrier in enterocytes is deficient.[8]
In humans the GLUT5 protein is encoded by the SLC2A5 gene.[9]
Regulation
Fructose uptake rate by GLUT5 is significantly affected by diabetes mellitus, hypertension, obesity, fructose malabsorption, and inflammation. However, age-related changes in fructose intake capability are not explained by the rate of expression of GLUT5.[10][11][12] The absorption of fructose in the simultaneous presence of glucose is improved, while sorbitol is inhibitory.[13]
Interactive pathway map
Click on genes, proteins and metabolites below to link to respective articles.[§ 1]
- ^ The interactive pathway map can be edited at WikiPathways: "GlycolysisGluconeogenesis_WP534".
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000142583 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000028976 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ Uldry M, Thorens B (February 2004). "The SLC2 family of facilitated hexose and polyol transporters" (PDF). Pflügers Archiv : European Journal of Physiology. 447 (5): 480–9. doi:10.1007/s00424-003-1085-0. PMID 12750891.
- ^ Hundal HS, Darakhshan F, Kristiansen S, Blakemore SJ, Richter EA (1998). "GLUT5 expression and fructose transport in human skeletal muscle". Advances in Experimental Medicine and Biology. 441: 35–45. doi:10.1007/978-1-4899-1928-1_4. ISBN 978-1-4899-1930-4. PMID 9781312.
- ^ Douard V, Ferraris RP (August 2008). "Regulation of the fructose transporter GLUT5 in health and disease". American Journal of Physiology. Endocrinology and Metabolism. 295 (2): E227–37. doi:10.1152/ajpendo.90245.2008. PMC 2652499. PMID 18398011.
- ^ Barone S, Fussell SL, Singh AK, Lucas F, Xu J, Kim C, Wu X, Yu Y, Amlal H, Seidler U, Zuo J, Soleimani M (February 2009). "Slc2a5 (Glut5) Is Essential for the Absorption of Fructose in the Intestine and Generation of Fructose-induced Hypertension". The Journal of Biological Chemistry. 284 (8): 5056–66. doi:10.1074/jbc.M808128200. PMC 2643499. PMID 19091748.
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: CS1 maint: unflagged free DOI (link) - ^ White PS, Jensen SJ, Rajalingam V, Stairs D, Sulman EP, Maris JM, Biegel JA, Wooster R, Brodeur GM (1998). "Physical mapping of the CA6, ENO1, and SLC2A5 (GLUT5) genes and reassignment of SLC2A5 to 1p36.2". Cytogenetics and Cell Genetics. 81 (1): 60–4. doi:10.1159/000014989. PMID 9691177.
- ^ Douard V, Ferraris RP (August 2008). "Regulation of the fructose transporter GLUT5 in health and disease". Am. J. Physiol. Endocrinol. Metab. 295 (2): E227–37. doi:10.1152/ajpendo.90245.2008. PMC 2652499. PMID 18398011.
- ^ Litherland GJ, Hajduch E, Gould GW, Hundal HS (June 2004). "Fructose transport and metabolism in adipose tissue of Zucker rats: diminished GLUT5 activity during obesity and insulin resistance" (PDF). Mol. Cell. Biochem. 261 (1–2): 23–33. doi:10.1023/b:mcbi.0000028734.77867.d2. PMID 15362482.
- ^ Drozdowski LA, Woudstra TD, Wild GE, Clandinin MT, Thomson AB (October 2004). "Age-associated changes in intestinal fructose uptake are not explained by alterations in the abundance of GLUT5 or GLUT2". J. Nutr. Biochem. 15 (10): 630–7. doi:10.1016/j.jnutbio.2004.06.003. PMID 15542355.
- ^ Heinrich Kasper: Ernährungsmedizin und Diätetik. 11. Auflage, Elsevier, Urban&Fischer-Verlag, 2009, ISBN 9783437420122, S. 208
External links
- GLUT5+Protein at the U.S. National Library of Medicine Medical Subject Headings (MeSH)