The Brain Hypometabolism Hypothesis Part 31: GLUT 9 and Urate


Professors Bernard Thorens and Mike Mueckler have written a review titled ‘Glucose Transporters in the 21st Century’. In terms of a Brain Hypometabolism Hypothesis, it is important to understand how Glucose is handled in the brain. Thorens and Mueckler reference 14 Glucose Transporters.

In their paper, Thorens and Mueckler discuss evidence to suggest that GLUT 9 is a urate transporter and is implicated in hyperuricaemia which can lead to Gout and is also seen in Lesch-Nyhan syndrome.

In terms of a hypothesis about metabolism this may not be relevant. Urate is an end-product of Purine metabolism and is usually excreted. Possibly the only significance here is that there is a conserved mechanism for molecular transport that is shared by metabolites such as Glucose. Nevertheless there is this paper which suggests that Urate may be neuroprotective (although high levels can also cause neuronal damage). There are also lines of evidence suggesting a possible interaction between Insulin and Urate.

As with other substrates the body has elegant mechanisms for homeostasis.

Appendix A – Citations

Bell S, Kolobova I, Crapper L, Ernst C, Lesch-Nyhan Syndrome: Models, Theories, and Therapies. Mol Syndromol 2016;7:302-311
Thorens B, Mueckler M. Glucose transporters in the 21st Century. American Journal of Physiology – Endocrinology and Metabolism. 2010;298(2):E141-E145. doi:10.1152/ajpendo.00712.2009.
Tomioka NH, Tamura Y, Takada T, Shibata S, Suzuki H, Uchida S, Hosoyamada M. Immunohistochemical and in situ hybridization study of urate transporters
GLUT9/URATv1, ABCG2, and URAT1 in the murine brain. Fluids Barriers CNS. 2016 Dec 12;13(1):22.

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