Central 5-HTR2C in the Control of Metabolic Homeostasis
The 5-hydroxytryptamine 2C receptor (5-HTR2C) is a class G protein-coupled receptor (GPCR) enriched in the hypothalamus and the brain stem, where it has been shown to regulate energy homeostasis, including feeding and glucose metabolism. Accordingly, 5-HTR2C has been the target of several anti-obesi...
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Published in | Frontiers in endocrinology (Lausanne) Vol. 12; p. 694204 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
21.07.2021
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Subjects | |
Online Access | Get full text |
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Summary: | The 5-hydroxytryptamine 2C receptor (5-HTR2C) is a class G protein-coupled receptor (GPCR) enriched in the hypothalamus and the brain stem, where it has been shown to regulate energy homeostasis, including feeding and glucose metabolism. Accordingly, 5-HTR2C has been the target of several anti-obesity drugs, though the associated side effects greatly curbed their clinical applications. Dissecting the specific neural circuits of 5-HTR2C-expressing neurons and the detailed molecular pathways of 5-HTR2C signaling in metabolic regulation will help to develop better therapeutic strategies towards metabolic disorders. In this review, we introduced the regulatory role of 5-HTR2C in feeding behavior and glucose metabolism, with particular focus on the molecular pathways, neural network, and its interaction with other metabolic hormones, such as leptin, ghrelin, insulin, and estrogens. Moreover, the latest progress in the clinical research on 5-HTR2C agonists was also discussed. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 Reviewed by: Jin Kwon Jeong, George Washington University, United States; Lourdes Mounien, Aix-Marseille Université, France This article was submitted to Neuroendocrine Science, a section of the journal Frontiers in Endocrinology These authors have contributed equally to this work and share first authorship Edited by: Etienne Challet, Université de Strasbourg, France These authors have contributed equally to this work and share last authorship |
ISSN: | 1664-2392 1664-2392 |
DOI: | 10.3389/fendo.2021.694204 |