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Cellular and molecular cues of glucose sensing in the rat olfactory bulb

In the brain, glucose homeostasis of extracellular fluid is crucial to the point that systems specifically dedicated to glucose sensing are found in areas involved in energy regulation and feeding behavior. Olfaction is a major sensory modality regulating food consumption. Nutritional status in turn...

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Autores principales: Al Koborssy, Dolly, Palouzier-Paulignan, Brigitte, Salem, Rita, Thevenet, Marc, Romestaing, Caroline, Julliard, A. Karyn
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4212682/
https://www.ncbi.nlm.nih.gov/pubmed/25400540
http://dx.doi.org/10.3389/fnins.2014.00333
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author Al Koborssy, Dolly
Palouzier-Paulignan, Brigitte
Salem, Rita
Thevenet, Marc
Romestaing, Caroline
Julliard, A. Karyn
author_facet Al Koborssy, Dolly
Palouzier-Paulignan, Brigitte
Salem, Rita
Thevenet, Marc
Romestaing, Caroline
Julliard, A. Karyn
author_sort Al Koborssy, Dolly
collection PubMed
description In the brain, glucose homeostasis of extracellular fluid is crucial to the point that systems specifically dedicated to glucose sensing are found in areas involved in energy regulation and feeding behavior. Olfaction is a major sensory modality regulating food consumption. Nutritional status in turn modulates olfactory detection. Recently it has been proposed that some olfactory bulb (OB) neurons respond to glucose similarly to hypothalamic neurons. However, the precise molecular cues governing glucose sensing in the OB are largely unknown. To decrypt these molecular mechanisms, we first used immunostaining to demonstrate a strong expression of two neuronal markers of glucose-sensitivity, insulin-dependent glucose transporter type 4 (GLUT4), and sodium glucose co-transporter type 1 (SGLT1) in specific OB layers. We showed that expression and mapping of GLUT4 but not SGLT1 were feeding state-dependent. In order to investigate the impact of metabolic status on the delivery of blood-borne glucose to the OB, we measured extracellular fluid glucose concentration using glucose biosensors simultaneously in the OB and cortex of anesthetized rats. We showed that glucose concentration in the OB is higher than in the cortex, that metabolic steady-state glucose concentration is independent of feeding state in the two brain areas, and that acute changes in glycemic conditions affect bulbar glucose concentration alone. These data provide new evidence of a direct relationship between the OB and peripheral metabolism, and emphasize the importance of glucose for the OB network, providing strong arguments toward establishing the OB as a glucose-sensing organ.
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spelling pubmed-42126822014-11-14 Cellular and molecular cues of glucose sensing in the rat olfactory bulb Al Koborssy, Dolly Palouzier-Paulignan, Brigitte Salem, Rita Thevenet, Marc Romestaing, Caroline Julliard, A. Karyn Front Neurosci Nutrition In the brain, glucose homeostasis of extracellular fluid is crucial to the point that systems specifically dedicated to glucose sensing are found in areas involved in energy regulation and feeding behavior. Olfaction is a major sensory modality regulating food consumption. Nutritional status in turn modulates olfactory detection. Recently it has been proposed that some olfactory bulb (OB) neurons respond to glucose similarly to hypothalamic neurons. However, the precise molecular cues governing glucose sensing in the OB are largely unknown. To decrypt these molecular mechanisms, we first used immunostaining to demonstrate a strong expression of two neuronal markers of glucose-sensitivity, insulin-dependent glucose transporter type 4 (GLUT4), and sodium glucose co-transporter type 1 (SGLT1) in specific OB layers. We showed that expression and mapping of GLUT4 but not SGLT1 were feeding state-dependent. In order to investigate the impact of metabolic status on the delivery of blood-borne glucose to the OB, we measured extracellular fluid glucose concentration using glucose biosensors simultaneously in the OB and cortex of anesthetized rats. We showed that glucose concentration in the OB is higher than in the cortex, that metabolic steady-state glucose concentration is independent of feeding state in the two brain areas, and that acute changes in glycemic conditions affect bulbar glucose concentration alone. These data provide new evidence of a direct relationship between the OB and peripheral metabolism, and emphasize the importance of glucose for the OB network, providing strong arguments toward establishing the OB as a glucose-sensing organ. Frontiers Media S.A. 2014-10-29 /pmc/articles/PMC4212682/ /pubmed/25400540 http://dx.doi.org/10.3389/fnins.2014.00333 Text en Copyright © 2014 Al Koborssy, Palouzier-Paulignan, Salem, Thevenet, Romestaing and Julliard. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Nutrition
Al Koborssy, Dolly
Palouzier-Paulignan, Brigitte
Salem, Rita
Thevenet, Marc
Romestaing, Caroline
Julliard, A. Karyn
Cellular and molecular cues of glucose sensing in the rat olfactory bulb
title Cellular and molecular cues of glucose sensing in the rat olfactory bulb
title_full Cellular and molecular cues of glucose sensing in the rat olfactory bulb
title_fullStr Cellular and molecular cues of glucose sensing in the rat olfactory bulb
title_full_unstemmed Cellular and molecular cues of glucose sensing in the rat olfactory bulb
title_short Cellular and molecular cues of glucose sensing in the rat olfactory bulb
title_sort cellular and molecular cues of glucose sensing in the rat olfactory bulb
topic Nutrition
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4212682/
https://www.ncbi.nlm.nih.gov/pubmed/25400540
http://dx.doi.org/10.3389/fnins.2014.00333
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