Endocrinology and Metabolism

Nomenclature of the GLUT/SLC2A family of sugar/polyol transport facilitators

Hans-Georg Joost, Graeme I. Bell, James D. Best, Morris J. Birnbaum, Maureen J. Charron, Y. T. Chen, Holger Doege, David E. James, Harvey F. Lodish, Kelle H. Moley, Jeffrey F. Moley, Mike Mueckler, Suzanne Rogers, Annette Schürmann, Susumu Seino, Bernard Thorens


The recent identification of several additional members of the family of sugar transport facilitators (gene symbol SLC2A, protein symbol GLUT) has created a heterogeneous and, in part, confusing nomenclature. Therefore, this letter provides a summary of the family members and suggests a systematic nomenclature for SLC2A and GLUT symbols.

  • membrane transport
  • glucose transporters
  • glucose transporter genes

the entry of sugars into mammalian cells is catalyzed by a family of transport facilitators (gene symbol SLC2A, protein symbol GLUT) that are characterized by the presence of 12 membrane-spanning helices and several conserved sequence motifs (6, 7, 11, 12, 14). Recently, additional family members have been identified on the basis of sequence similarity (1-5, 8-10, 13,15-17). Because some of these novel transporters have been described independently by different groups, a heterogeneous and sometimes confusing nomenclature has developed. Therefore, herein we provide a summary of the known members of the family, along with their aliases and accession numbers, and we present a suggestion for a systematic nomenclature.

As is summarized in Table 1, it is suggested that a GLUT numbering scheme be used that is identical with the numbering of the genes in the SLC2A nomenclature of the sugar transporter genes as approved by the Human Genome Organization Gene Nomenclature Committee. According to this system, one of the proteins initially designated GLUT9 (2) was renamed GLUT6 (9). The symbol GLUT6 was previously used for a pseudogene (SLC2A3P) derived from the GLUT3 gene (11). However, it seems more appropriate to use this symbol for an expressed gene rather than a pseudogene. Note also that two transport facilitators that will now receive the symbols GLUT11 (SLC2A11, Ref. 4) and GLUT12 (SLC2A12) have been described in preliminary publications as GLUT10 (3) and GLUT8 (16), respectively. In addition, we suggest using the symbols GLUT8 (1, 5) and GLUT9 (15) rather than their aliases GLUTX1 (8) and GLUTX (16), respectively. Finally, the symbol GLUT7, which had previously been assigned to a now withdrawn sequence, will be used for one of the novel genes (SLC2A7).

View this table:
Table 1.

Summary of the extended GLUT family

According to a dendrogram depicting the sequence similarities (Fig. 1), the family can be divided into three subclasses. Class I is comprised of the extensively characterized glucose transporters GLUT1 to GLUT4, which can be distinguished on the basis of their distinct tissue distributions (GLUT1, erythrocytes, brain microvessels; GLUT2, liver, pancreatic islets; GLUT3, neuronal cells; GLUT4, muscle, adipose tissue) and their hormonal regulation (e.g., insulin sensitivity of GLUT4). Class II is comprised of the fructose-specific transporter GLUT5 and three related proteins, GLUT7, GLUT9, and GLUT11. For GLUT11, fructose-inhibitable glucose transport activity has been demonstrated in a system of reconstituted vesicles (4). Class III is characterized by the lack of a glycosylation site in the first extracellular linker domain and by the presence of such a site in loop 9. As is also shown in the tree, the recently cloned proton-myoinositol symporter (HMIT1, Ref. 18) can be included in the class III GLUTs (10). Glucose transport activity has been demonstrated for GLUT6 and GLUT8. It should be emphasized, however, that the designation of the family does not necessarily reflect the substrate specificity of its members, which may transport sugars or polyols other than glucose (e.g., GLUT5, fructose; HMIT1, myoinositol).

Fig. 1.

Dendrogram of a multiple alignment of all members of the extended GLUT family. The alignment was performed with the clustree program (Heidelberg UNIX sequence analysis resources package from the Deutsches Krebsforschungszentrum, Heidelberg, Germany). The results were corrected for multiple substitutions, and positions with gaps were excluded. Branch lengths reflect the degree of difference between the sequences. Reproduced from Ref. 10, with permission of Taylor & Francis Ltd.


  • Address for reprint requests and other correspondence: H.-G. Joost, Institut fuer Pharmakologie und Toxikologie, Medizinische Fakultaet der RWTH Aachen, Wendlingweg 2, 52057 Aachen, Germany (E-mail: joost{at}rwth-aachen.de).

  • The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

  • 10.1152/ajpendo.00407.2001


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