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The Journal of Neuroscience, November 1, 2002, 22(21):9160-9165

BRIEF COMMUNICATION
Past-A, a Novel Proton-Associated Sugar Transporter, Regulates Glucose Homeostasis in the Brain

Noriaki Shimokawa^{1, 2, 3}, Junichi Okada^{2, 3}, Kaisa Haglund¹, Ivan Dikic¹, Noriyuki Koibuchi^{2, 3}, and Mitsuhiko Miura²

¹ Molecular Signaling Group, Ludwig Institute for Cancer Research, Uppsala, S-75124, Sweden, ² Department of Physiology First Division, Gunma University School of Medicine, Maebashi-shi 371-8511, Japan, and ³  Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Kawaguchi, Saitama 332-0012, Japan

The ventral medullary surface (VMS) of the medulla oblongata is known to be the site of the central chemosensitive neurons in mammals. These neurons sense excess H⁺/CO₂ dissolved in the CSF and induce hyperventilation. To elucidate the mechanism of neuronal cell adaptation to changes of H⁺/CO₂, we screened for hypercapnia-induced genes in the VMS. Here, we report cloning and characterization of a novel gene called proton-associated sugar transporter-A (Past-A), which is induced in the brain after hypercapnia and mediates glucose uptake along the pH gradient. Past-A comprises 751 amino acid residues containing 12 membrane-spanning helices, several conserved sugar transport motifs, three proline-rich regions, and leucine repeats. Past-A transcript was expressed predominantly in the brain. Moreover, the Past-A-immunoreactive neural cells were found in the VMS of the medulla oblongata, and the number of immunoreactive cells was increased by hypercapnic stimulation. Transient transfection of Past-A in COS-7 cells leads to the expression of a membrane-associated 82 kDa protein that possesses a glucose transport activity. The acidification of extracellular medium facilitated glucose uptake, whereas the addition of carbonyl cyanide m-chlorophenylhydrazone, a protonophore, inhibited glucose import. Together, our results indicate that Past-A is a brain-specific glucose transporter that may represent an adaptation mechanism regulating sugar homeostasis in neuronal cells after hypercapnia.

Key words: differential display; hypercapnia-induced gene; proton-associated sugar transporter; glucose uptake; ventral medullary surface; glucose homeostasis

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22219160-06$05.00/0

This article has been cited by other articles:

				S. J. Gatley Labeled Glucose Analogs in the Genomic Era J. Nucl. Med., July 1, 2003; 44(7): 1082 - 1086. [Full Text] [PDF]

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