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Sweet taste signaling functions as a hypothalamic glucose sensor

July 12, 2009

When animals were fasted 24 hours, two taste receptor genes’ expression increased in specific brain regions.
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Ren X, Zhou L, Terwilliger R, Newton SS, de Araujo IE. Front Integr Neurosci. 2009;3:12. Epub 2009 Jun 19. PMID: 19587847
http://tinyurl.com/lf9rva

Brain glucosensing is essential for normal body glucose homeostasis and
neuronal function. However, the exact signaling mechanisms involved in the
neuronal sensing of extracellular glucose levels remain poorly understood.
Of particular interest is the identification of candidate membrane molecular
sensors that would allow neurons to change firing rates independently of
intracellular glucose metabolism.

Here we describe for the first time the expression of the taste receptor
genes Tas1r1, Tas1r2 and Tas1r3, and their associated G-protein genes, in
the mammalian brain. Neuronal expression of taste genes was detected in
different nutrient-sensing forebrain regions, including the paraventricular
and arcuate nuclei of the hypothalamus, the CA fields and dentate gyrus of
the hippocampus, the habenula, and cortex. Expression was also observed in
the intra-ventricular epithelial cells of the choroid plexus. These same
regions were found to express the corresponding gene products that form the
heterodimeric T1R2/T1R3 and T1R1/T1R3 sweet and l-amino acid taste G-protein
coupled receptors, respectively, along with the taste G-protein
alpha-gustducin. Moreover, in vivo studies in mice demonstrated that the
hypothalamic expression of taste-related genes is regulated by the
nutritional state of the animal, with food deprivation significantly
increasing expression levels of Tas1r1 and Tas1r2 in hypothalamus, but not
in cortex. Furthermore, exposing mouse hypothalamic cells to a low-glucose
medium, while maintaining normal l-amino acid concentrations, specifically
resulted in higher expression levels of the sweet-associated gene Tas1r2.
This latter effect was reversed by adding the non-metabolizable artificial
sweetener sucralose to the low-glucose medium, indicating that taste-like
signaling in hypothalamic neurons does not require intracellular glucose
oxidation.

Taken together, our findings suggest that the heterodimeric G-protein
coupled sweet receptor T1R2/T1R3 is a candidate membrane-bound brain
glucosensor.

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