Glial hypothalamic inhibition of glut2 expression alters satiety, impacting eating behavior
Autor: | Magdiel Salgado, María De Los Ángeles García-Robles, Kathleen Escobar-Acuña, Fernando J. Sepúlveda, Roberto Elizondo-Vega, Antonia Recabal, Ricardo C. Araneda, Elena Uribe, María José Barahona, Patricio Ordenes, Paula Llanos |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Male medicine.medical_specialty endocrine system Central nervous system Hypothalamus Neuropeptide Satiation Rats Sprague-Dawley tanycytes 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Orexigenic Internal medicine medicine Animals RNA Messenger Cells Cultured Research Articles Glucose Transporter Type 2 Gene knockdown biology glucosensing Body Weight Neuropeptides knockdown Fasting Feeding Behavior Autonomic nervous system 030104 developmental biology Endocrinology medicine.anatomical_structure Neurology Gene Knockdown Techniques biology.protein GLUT2 Brainstem Neuroglia 030217 neurology & neurosurgery medicine.drug Brain Stem Research Article |
Zdroj: | Glia Artículos CONICYT CONICYT Chile instacron:CONICYT |
Popis: | Glucose 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. |
Databáze: | OpenAIRE |
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