GLUT1

GLUT1 was the first glucose transporter to be characterized. [cite journal |author=Mueckler M, Caruso C, Baldwin SA, "et al" |title=Sequence and structure of a human glucose transporter |journal=Science |volume=229 |issue=4717 |pages=941–5 |year=1985 |pmid=3839598 |doi=] It is widely distributed in fetal tissues. In the adult it is expressed at highest levels in erythrocytes and also in the endothelial cells of barrier tissues such as the blood-brain barrier. Glut1 is a major receptor for take-up of Vitamin C as well as glucose, especially in non vitamin C producing mammals as part of an adaptation to compensate by participating in a Vitamin C recycling process. In mammals that do produce Vitamin C Glut4 is often expressed instead of Glut1.cite journal | author = Montel-hagen A, Kinet S, Manel N "et al" | year = 2008 | title = Erythrocyte Glut1 Triggers Dehydroascorbic Acid Uptake in Mammals Unable to Synthesize Vitamin C | journal = Cell | volume = 132 | issue = 6 | pages = 1039–1048 | doi = 10.1016/j.cell.2008.01.042 | laysummary = http://www.sciencedaily.com/releases/2008/03/080320120726.htm | laysource = ScienceDaily | laydate = 2008-03-21]

tructure

GLUT1 behaves as a Michaelis-Menten enzyme and contains 12 membrane-spanning alpha helices, each containing 20 amino acid residues. A helical wheel analysis shows that the membrane spanning alpha helices are amphipathic, with one side being polar and the other side hydrophobic. Six of these membrane spanning helices are believed to bind together in the membrane to create a polar channel in the center through which glucose can traverse, with the hydrophobic regions on the outside of the channel adjacent to the fatty acid tails of the membrane.

Pathology

Mutations in the GLUT1 gene are responsible for GLUT1 deficiency or De Vivo disease, which is a rare autosomal dominant disorder. [cite journal |author=Seidner G, Alvarez MG, Yeh JI, "et al" |title=GLUT-1 deficiency syndrome caused by haploinsufficiency of the blood-brain barrier hexose carrier |journal=Nat. Genet. |volume=18 |issue=2 |pages=188–91 |year=1998 |pmid=9462754 |doi=10.1038/ng0298-188] This disease is characterized by a low cerebrospinal fluid glucose concentration (hypoglycorrhachia) which results from impaired glucose transport across the blood-brain barrier.

Role in HTLV infection

GLUT1 is also a receptor used by the HTLV virus to gain entry into target cells. [cite journal |author=Manel N, Kim FJ, Kinet S, Taylor N, Sitbon M, Battini JL |title=The ubiquitous glucose transporter GLUT-1 is a receptor for HTLV |journal=Cell |volume=115 |issue=4 |pages=449–59 |year=2003 |month=November |pmid=14622599 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S009286740300881X]

References

Further reading

PBB_Further_reading
citations =
*cite journal | author=Hruz PW, Mueckler MM |title=Structural analysis of the GLUT1 facilitative glucose transporter (review). |journal=Mol. Membr. Biol. |volume=18 |issue= 3 |pages= 183–93 |year= 2002 |pmid= 11681785 |doi=
*cite journal | author=Baumann MU, Deborde S, Illsley NP |title=Placental glucose transfer and fetal growth. |journal=Endocrine |volume=19 |issue= 1 |pages= 13–22 |year= 2003 |pmid= 12583599 |doi=
*cite journal | author=Mobasheri A, Richardson S, Mobasheri R, "et al." |title=Hypoxia inducible factor-1 and facilitative glucose transporters GLUT1 and GLUT3: putative molecular components of the oxygen and glucose sensing apparatus in articular chondrocytes. |journal=Histol. Histopathol. |volume=20 |issue= 4 |pages= 1327–38 |year= 2006 |pmid= 16136514 |doi=

External links

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