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Ann Neurol. 1998 Aug;44(2):286-7.

Deficient transport of dehydroascorbic acid in the glucose transporter protein syndrome.

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1
Neurological Institute, Columbia University, New York, NY 10032, USA.

Abstract

The glucose transporter protein syndrome (GTPS) is caused by defective transport of glucose across the blood-brain barrier via the glucose transporter GLUT1, resulting in hypoglycorrhachia, infantile seizures, and developmental delay. Recent reports indicated that GLUT1 is a multifunctional transporter. We investigated the transport of vitamin C in its oxidized form (dehydroascorbic acid) via GLUT1 into erythrocytes of 2 patients with GTPS. In both patients, uptake of oxidized vitamin C was 61% of the mothers' values. Our findings are consistent with recent observations that vitamin C is transported in its oxidized form via GLUT1. We speculate that impaired transport of this substrate and perhaps other substrates in GTPS might contribute to the pathophysiology of this condition.

PMID:
9708557
DOI:
10.1002/ana.410440225
[Indexed for MEDLINE]
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