Glut3: Difference between revisions

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Kevin Keaveney, Miranda Moore, Javier Blanco, Lainey Scarvey, Samantha Chinn, Michal Harel, Matthew J Lowry

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 Higher glucose concentration, as seen in diabetics, influences GLUT expression in leukocytes. Patients with type 2 diabetes have decreased GLUT3 in granulocytes, lymphocytes, and monocytes.  In addition, the level of transcripts that encode GLUT3 are reduced in diabetic patients.  Decreased expression of GLUT3 and other GLUT isoforms could possibly impair immune function and increase susceptibility to infection in type 2 diabetes<ref name="four"/>.
 ===Alzheimer's Disease===
-Alzheimer’s disease shows levels of impaired glucose uptake and metabolism, which leads to lead to neurodegeneration via down-regulation of many other factors in the brain. GLUT3 is responsible for transporting glucose from extracellular space to neuronal tissue, specifically dendrites and axons. Decreased levels of GLUT3 in Alzheimer brain shows a positive correlation to decreased levels of N-acetylglucosamine, which is a derivative of glucose. The impaired presence of GLUT3 leads to hyperphosphorylation of the Tau protein, which normally stabilizes neuronal microtubules. Lastly there is a reduction in the transcription for factor hypoxia-inducible factor 1, which plays a role in glucose metabolism in the brain. The comparison between a normal healthy brain and an Alzheimer brain revealed that there was a 25-30% decrease in GLUT3 levels in the Alzheimer brain<ref name="eight"/>.
+Alzheimer’s disease shows levels of impaired glucose uptake and metabolism, which leads to neurodegeneration via down-regulation of many other factors in the brain. GLUT3 is responsible for transporting glucose from extracellular space to neuronal tissue, specifically dendrites and axons. Decreased levels of GLUT3 in Alzheimer brain shows a positive correlation to decreased levels of N-acetylglucosamine, which is a derivative of glucose. The impaired presence of GLUT3 leads to hyperphosphorylation of the Tau protein, which normally stabilizes neuronal microtubules. Lastly there is a reduction in the transcription for factor hypoxia-inducible factor 1, which plays a role in glucose metabolism in the brain. The comparison between a normal healthy brain and an Alzheimer brain revealed that there was a 25-30% decrease in GLUT3 levels in the Alzheimer brain<ref name="eight"/>.
 ===Huntington’s Disease===
 Huntington’s disease leads to decreased expression of GLUT3 in the plasma membrane. Increasing the expression of GLUT3 in a Huntington’s disease brain can delay the onset of the disease<ref name="ten">Vittori, A., Breda, C., Repici, M., Orth, M., Roos, R. A. C., Outeiro, T. F., . . . the REGISTRY investigators of the European Huntington's Disease Network. (2014). Copy-number variation of the neuronal glucose transporter gene SLC2A3 and age of onset in huntington's disease. Human Molecular Genetics, 23(12), 3129-3137. doi:10.1093/hmg/ddu022</ref>. Rab11 is a protein that is involved with the regulation of transporter trafficking. It helps in the regulation of glucose transporters particularly the GLUT3 transporter. Its regulation is impaired by Huntington’s disease, which leads to the decreased cell surface expression of GLUT3 in the brain. The exact mechanism of Huntington’s disease is still unknown to this day<ref name="eleven">McClory, H., Williams, D., & Sapp, E. (2014). Glucose transporter 3 is a rab11-dependent trafficking cargo and its transport to the cell surface is reduced in neurons of CAG140 Huntington’s disease mice. Acta Neuropathol Commun, 2, 1-9.</ref>.