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Int. J. Mol. Sci. 2012, 13(10), 12629-12655; doi:10.3390/ijms131012629

The Role of Glucose Transporters in Brain Disease: Diabetes and Alzheimer’s Disease

Department of Pharmaceutical Sciences, School of Pharmacy, Texas Tech University Health Sciences Center, 1300 S. Coulter Street, Amarillo, TX 79106, USA
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Received: 1 August 2012 / Revised: 19 September 2012 / Accepted: 24 September 2012 / Published: 3 October 2012
(This article belongs to the Special Issue Neuroprotective Strategies 2012)
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Abstract

The occurrence of altered brain glucose metabolism has long been suggested in both diabetes and Alzheimer’s diseases. However, the preceding mechanism to altered glucose metabolism has not been well understood. Glucose enters the brain via glucose transporters primarily present at the blood-brain barrier. Any changes in glucose transporter function and expression dramatically affects brain glucose homeostasis and function. In the brains of both diabetic and Alzheimer’s disease patients, changes in glucose transporter function and expression have been observed, but a possible link between the altered glucose transporter function and disease progress is missing. Future recognition of the role of new glucose transporter isoforms in the brain may provide a better understanding of brain glucose metabolism in normal and disease states. Elucidation of clinical pathological mechanisms related to glucose transport and metabolism may provide common links to the etiology of these two diseases. Considering these facts, in this review we provide a current understanding of the vital roles of a variety of glucose transporters in the normal, diabetic and Alzheimer’s disease brain. View Full-Text
Keywords: glucose transporter; GLUT; SGLT; diabetes; Alzheimer’s disease; blood brain barrier; glucose metabolism glucose transporter; GLUT; SGLT; diabetes; Alzheimer’s disease; blood brain barrier; glucose metabolism
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Shah, K.; DeSilva, S.; Abbruscato, T. The Role of Glucose Transporters in Brain Disease: Diabetes and Alzheimer’s Disease. Int. J. Mol. Sci. 2012, 13, 12629-12655.

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