Glial hypothalamic inhibition of GLUT2 expression alters satiety, impacting eating behavior

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dc.contributor.authorBarahona, María J.
dc.contributor.authorLlanos, Paula
dc.contributor.authorRecabal, Antonia
dc.contributor.authorEscobar-Acuña, Kathleen
dc.contributor.authorElizondo-Vega, Roberto
dc.contributor.authorSalgado, Magdiel
dc.contributor.authorOrdenes, Patricio
dc.contributor.authorUribe, Elena
dc.contributor.authorSepúlveda, Fernando J.
dc.contributor.authorAraneda, Ricardo C.
dc.contributor.authorGarcía-Robles, María A.
dc.date.accessioned2022-08-30T18:09:28Z
dc.date.available2022-08-30T18:09:28Z
dc.date.issued2018-03
dc.descriptionIndexación Scopuses
dc.description.abstractGlucose is a key modulator of feeding behavior. By acting in peripheral tissues and in the central nervous system, it directly controls the secretion of hormones and neuropeptides and modulates the activity of the autonomic nervous system. GLUT2 is required for several glucoregulatory responses in the brain, including feeding behavior, and is localized in the hypothalamus and brainstem, which are the main centers that control this behavior. In the hypothalamus, GLUT2 has been detected in glial cells, known as tanycytes, which line the basal walls of the third ventricle (3V). This study aimed to clarify the role of GLUT2 expression in tanycytes in feeding behavior using 3V injections of an adenovirus encoding a shRNA against GLUT2 and the reporter EGFP (Ad-shGLUT2). Efficient in vivo GLUT2 knockdown in rat hypothalamic tissue was demonstrated by qPCR and Western blot analyses. Specificity of cell transduction in the hypothalamus and brainstem was evaluated by EGFP-fluorescence and immunohistochemistry, which showed EGFP expression specifically in ependymal cells, including tanycytes. The altered mRNA levels of both orexigenic and anorexigenic neuropeptides suggested a loss of response to increased glucose in the 3V. Feeding behavior analysis in the fasting-feeding transition revealed that GLUT2-knockdown rats had increased food intake and body weight, suggesting an inhibitory effect on satiety. Taken together, suppression of GLUT2 expression in tanycytes disrupted the hypothalamic glucosensing mechanism, which altered the feeding behavior. © 2017 The Authors GLIA Published by Wiley Periodicals, Inc.es
dc.description.urihttps://onlinelibrary-wiley-com.recursosbiblioteca.unab.cl/doi/10.1002/glia.23267
dc.identifier.citationGLIA Volume 66, Issue 3, Pages 592 - 605March 2018es
dc.identifier.doi10.1002/glia.23267
dc.identifier.issn08941491
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/23670
dc.language.isoenes
dc.publisherJohn Wiley and Sons Inc.es
dc.rights.licenseCC BY-NC
dc.subjectRhombencephalones
dc.subjectGlucosees
dc.subjectHypoglycemiaes
dc.subjectKnockdownes
dc.subjectTanycyteses
dc.titleGlial hypothalamic inhibition of GLUT2 expression alters satiety, impacting eating behaviores
dc.typeArtículoes
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