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Appetite Regulation of TLR4-Induced Inflammatory Signaling

Appetite is the basis for obtaining food and maintaining normal metabolism. Toll-like receptor 4 (TLR4) is an important receptor expressed in the brain that induces inflammatory signaling after activation. Inflammation is considered to affect the homeostatic and non-homeostatic systems of appetite,...

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Detalles Bibliográficos
Autores principales: Li, Yongxiang, Jiang, Qingyan, Wang, Lina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8664591/
https://www.ncbi.nlm.nih.gov/pubmed/34899611
http://dx.doi.org/10.3389/fendo.2021.777997
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author Li, Yongxiang
Jiang, Qingyan
Wang, Lina
author_facet Li, Yongxiang
Jiang, Qingyan
Wang, Lina
author_sort Li, Yongxiang
collection PubMed
description Appetite is the basis for obtaining food and maintaining normal metabolism. Toll-like receptor 4 (TLR4) is an important receptor expressed in the brain that induces inflammatory signaling after activation. Inflammation is considered to affect the homeostatic and non-homeostatic systems of appetite, which are dominated by hypothalamic and mesolimbic dopamine signaling. Although the pathological features of many types of inflammation are known, their physiological functions in appetite are largely unknown. This review mainly addresses several key issues, including the structures of the homeostatic and non-homeostatic systems. In addition, the mechanism by which TLR4-induced inflammatory signaling contributes to these two systems to regulate appetite is also discussed. This review will provide potential opportunities to develop new therapeutic interventions that control appetite under inflammatory conditions.
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spelling pubmed-86645912021-12-11 Appetite Regulation of TLR4-Induced Inflammatory Signaling Li, Yongxiang Jiang, Qingyan Wang, Lina Front Endocrinol (Lausanne) Endocrinology Appetite is the basis for obtaining food and maintaining normal metabolism. Toll-like receptor 4 (TLR4) is an important receptor expressed in the brain that induces inflammatory signaling after activation. Inflammation is considered to affect the homeostatic and non-homeostatic systems of appetite, which are dominated by hypothalamic and mesolimbic dopamine signaling. Although the pathological features of many types of inflammation are known, their physiological functions in appetite are largely unknown. This review mainly addresses several key issues, including the structures of the homeostatic and non-homeostatic systems. In addition, the mechanism by which TLR4-induced inflammatory signaling contributes to these two systems to regulate appetite is also discussed. This review will provide potential opportunities to develop new therapeutic interventions that control appetite under inflammatory conditions. Frontiers Media S.A. 2021-11-24 /pmc/articles/PMC8664591/ /pubmed/34899611 http://dx.doi.org/10.3389/fendo.2021.777997 Text en Copyright © 2021 Li, Jiang and Wang https://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) and the copyright owner(s) 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 Endocrinology
Li, Yongxiang
Jiang, Qingyan
Wang, Lina
Appetite Regulation of TLR4-Induced Inflammatory Signaling
title Appetite Regulation of TLR4-Induced Inflammatory Signaling
title_full Appetite Regulation of TLR4-Induced Inflammatory Signaling
title_fullStr Appetite Regulation of TLR4-Induced Inflammatory Signaling
title_full_unstemmed Appetite Regulation of TLR4-Induced Inflammatory Signaling
title_short Appetite Regulation of TLR4-Induced Inflammatory Signaling
title_sort appetite regulation of tlr4-induced inflammatory signaling
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8664591/
https://www.ncbi.nlm.nih.gov/pubmed/34899611
http://dx.doi.org/10.3389/fendo.2021.777997
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