ArticleScientific reports2022
GLUT2 expression by glial fibrillary acidic protein-positive tanycytes is required for promoting feeding-response to fasting.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Tanycytes: bloodhounds of the metabolic brain.Trends in endocrinology and metabolism: TEM · 2026Review
- Methodological Challenges for Ablation of BMPR1A in Hypothalamic Tanycytes-A Cautionary Tale.FASEB bioAdvances · 2026Article
- Tanycytic G6PT silencing prevents obesity induced by early postnatal overnutrition.Scientific reports · 2026Article
- The unanticipated role of the glial-associated glucose-6-phosphatase system in brain homeostasis.iScience · 2025Review
- Hindbrain Lactoprivic Regulation of Hypothalamic Third Ventricular Alpha-2 Tanycyte Metabolic Sensor Gene Expression in Hypoglycemic Male Versus Female Rats.Neurochemical research · 2025Article
- Knocking down the neuronal lactate transporter MCT2 in the arcuate nucleus of female rats increases food intake and body weight.Scientific reports · 2025Article
- Fasting induces metabolic switches and spatial redistributions of lipid processing and neuronal interactions in tanycytes.Nature communications · 2024Article
- Glucose transporter-2 regulation of VMN GABA neuron metabolic sensor and transmitter gene expression.Scientific reports · 2024Article
- Saturated fatty acids stimulate cytokine production in tanycytes via the PP2Ac-dependent signaling pathway.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- The influence of extended fasting on thyroid hormone: local and differentiated regulatory mechanisms.Frontiers in endocrinology · 2024Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Feeding behavior is a complex process that depends on the ability of the brain to integrate hormonal and nutritional signals, such as glucose. One glucosensing mechanism relies on the glucose transporter 2 (GLUT2) in the hypothalamus, especially in radial glia-like cells called tanycytes. Here, we analyzed whether a GLUT2-dependent glucosensing mechanism is required for the normal regulation of feeding behavior in GFAP-positive tanycytes. Genetic inactivation of Glut2 in GFAP-expressing tanycytes was performed using Cre/Lox technology. The efficiency of GFAP-tanycyte targeting was analyzed in the anteroposterior and dorsoventral axes by evaluating GFP fluorescence. Feeding behavior, hormonal levels, neuronal activity using c-Fos, and neuropeptide expression were also analyzed in the fasting-to-refeeding transition. In basal conditions, Glut2-inactivated mice had normal food intake and meal patterns. Implementation of a preceeding fasting period led to decreased total food intake and a delay in meal initiation during refeeding. Additionally, Glut2 inactivation increased the number of c-Fos-positive cells in the ventromedial nucleus in response to fasting and a deregulation of Pomc expression in the fasting-to-refeeding transition. Thus, a GLUT2-dependent glucose-sensing mechanism in GFAP-tanycytes is required to control food consumption and promote meal initiation after a fasting period.
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