Cited by 268Biochemical Analysis and Sensing TechniquesRegulation of Appetite and ObesityIon Channels and Receptors

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Sweet taste signaling functions as a hypothalamic glucose sensor

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Ren, Xueying·2009·Frontiers in Integrative Neuroscience

DOI 10.3389/neuro.07.012.2009PMC PMC2706652

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Abstract

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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Authors: Ren, X.
Affiliations: Yale University (US)
Corresponding author: Ren, Xueying
ORCID: Ren, Xueying
Venue: Frontiers in Integrative Neuroscience
Publisher: Frontiers Media SA
Published: 2009
Volume: 3
Pages: 12-12
ISSN: 1662-5145 (ISSN-L)
DOI: 10.3389/neuro.07.012.2009
PMC: PMC2706652
OpenAlex: W2018768372
Cited by: 267
References: 48
Citations by year: 2026: 6 · 2025: 12 · 2024: 14 · 2023: 13 · 2022: 16 · 2021: 16 · 2020: 11 · 2019: 11 · 2018: 20 · 2017: 25 · 2016: 19 · 2015: 17 · 2014: 19 · 2013: 15 · 2012: 15
FWCI: 17.10
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Frontiers in Integrative Neuroscience (publishedVersion, cc-by)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
MPG.PuRe (Max Planck Society) (submittedVersion)
Topics: Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords: hypothalamus, sweet taste receptor, T1R2/T1R3, TAS1R2, TAS1R1, TAS1R3, gustducin, glucose homeostasis, food deprivation, sucralose

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Sweet taste signaling functions as a hypothalamic glucose sensor

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