CaMK1D signaling in AgRP neurons promotes ghrelin-mediated food intake

التفاصيل البيبلوغرافية
العنوان: CaMK1D signaling in AgRP neurons promotes ghrelin-mediated food intake
المؤلفون: Vivot, Kevin, Meszaros, Gergö, Zhang, Zhirong, Erbs, Eric, Yeghiazaryan, Gagik, Quiñones, Mar, Grandgirard, Erwan, Schneider, Anna, Clauss--Creusot, Etienne, Charlet, Alexandre, Faour, Maya, Martin, Claire, Luquet, Serge, Kloppenburg, Peter, Nogueiras, Ruben, Ricci, Romeo
المساهمون: Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), University of Cologne, Instituto de Investigación Sanitaria de Santiago de Compostela / Health Research Institute of Santiago de Compostela (IDIS), CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III Madrid (ISC), Institut des Neurosciences Cellulaires et Intégratives (INCI), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Unité de Biologie Fonctionnelle et Adaptative (BFA (UMR_8251 / U1133)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité)
المصدر: https://hal.science/hal-03795873Test ; 2022.
بيانات النشر: HAL CCSD
سنة النشر: 2022
المجموعة: Archive ouverte HAL (Hyper Article en Ligne, CCSD - Centre pour la Communication Scientifique Directe)
مصطلحات موضوعية: [SDV]Life Sciences [q-bio]
الوصف: Hypothalamic AgRP/NPY neurons are key players in the control of feeding behavior. Ghrelin, a major hormone released under fasting conditions, activates orexigenic AgRP/NPY neurons to stimulate food intake and adiposity. However, cell-autonomous ghrelin-dependent signaling mechanisms in AgRP/NPY neurons remain poorly defined. Here we demonstrate that calcium/calmodulin-dependent protein kinase ID (CaMK1D), a genetic hot spot in type 2 diabetes, is activated in hypothalamus upon ghrelin stimulation and acts in AgRP neurons to promote ghrelin-dependent food intake. Global CaMK1D knockout mice are resistant to the orexigenic action of ghrelin, gain less body weight and are protected against high-fat dietinduced obesity. Deletion of CaMK1D in AgRP but not in POMC neurons is sufficient to recapitulate above phenotypes. Lack of CaMK1D attenuates phosphorylation of CREB and CREB-dependent expression of the orexigenic neuropeptides AgRP/NPY as well as the amount of AgRP fiber projections to the Paraventricular nucleus (PVN), while electrical activity of AgRP neurons and 5' AMP-activated protein kinase (AMPK) signaling are unaffected. Hence, CaMK1D links ghrelin action to transcriptional control of orexigenic neuropeptide availability in AgRP neurons.
نوع الوثيقة: report
اللغة: English
العلاقة: hal-03795873; https://hal.science/hal-03795873Test; https://hal.science/hal-03795873/documentTest; https://hal.science/hal-03795873/file/Vivot%20et%20al.%20Nature%20Metabolism.pdfTest
الإتاحة: https://hal.science/hal-03795873Test
https://hal.science/hal-03795873/documentTest
https://hal.science/hal-03795873/file/Vivot%20et%20al.%20Nature%20Metabolism.pdfTest
حقوق: info:eu-repo/semantics/OpenAccess
رقم الانضمام: edsbas.74D02F4C
قاعدة البيانات: BASE
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