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Insulin Signaling in Arthritis

Inflammatory arthritis is burdened by an increased risk of metabolic disorders. Cytokines and other mediators in inflammatory diseases lead to insulin resistance, diabetes and hyperlipidemia. Accumulating evidence in the field of immunometabolism suggests that the cause-effect relationship between a...

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Autores principales: Tripolino, Cesare, Ciaffi, Jacopo, Pucino, Valentina, Ruscitti, Piero, van Leeuwen, Nina, Borghi, Claudio, Giacomelli, Roberto, Meliconi, Riccardo, Ursini, Francesco
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8119635/
https://www.ncbi.nlm.nih.gov/pubmed/33995414
http://dx.doi.org/10.3389/fimmu.2021.672519
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author Tripolino, Cesare
Ciaffi, Jacopo
Pucino, Valentina
Ruscitti, Piero
van Leeuwen, Nina
Borghi, Claudio
Giacomelli, Roberto
Meliconi, Riccardo
Ursini, Francesco
author_facet Tripolino, Cesare
Ciaffi, Jacopo
Pucino, Valentina
Ruscitti, Piero
van Leeuwen, Nina
Borghi, Claudio
Giacomelli, Roberto
Meliconi, Riccardo
Ursini, Francesco
author_sort Tripolino, Cesare
collection PubMed
description Inflammatory arthritis is burdened by an increased risk of metabolic disorders. Cytokines and other mediators in inflammatory diseases lead to insulin resistance, diabetes and hyperlipidemia. Accumulating evidence in the field of immunometabolism suggests that the cause-effect relationship between arthritis and metabolic abnormalities might be bidirectional. Indeed, the immune response can be modulated by various factors such as environmental agents, bacterial products and hormones. Insulin is produced by pancreatic cells and regulates glucose, fat metabolism and cell growth. The action of insulin is mediated through the insulin receptor (IR), localized on the cellular membrane of hepatocytes, myocytes and adipocytes but also on the surface of T cells, macrophages, and dendritic cells. In murine models, the absence of IR in T-cells coincided with reduced cytokine production, proliferation, and migration. In macrophages, defective insulin signaling resulted in enhanced glycolysis affecting the responses to pathogens. In this review, we focalize on the bidirectional cause-effect relationship between impaired insulin signaling and arthritis analyzing how insulin signaling may be involved in the aberrant immune response implicated in arthritis and how inflammatory mediators affect insulin signaling. Finally, the effect of glucose-lowering agents on arthritis was summarized.
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spelling pubmed-81196352021-05-15 Insulin Signaling in Arthritis Tripolino, Cesare Ciaffi, Jacopo Pucino, Valentina Ruscitti, Piero van Leeuwen, Nina Borghi, Claudio Giacomelli, Roberto Meliconi, Riccardo Ursini, Francesco Front Immunol Immunology Inflammatory arthritis is burdened by an increased risk of metabolic disorders. Cytokines and other mediators in inflammatory diseases lead to insulin resistance, diabetes and hyperlipidemia. Accumulating evidence in the field of immunometabolism suggests that the cause-effect relationship between arthritis and metabolic abnormalities might be bidirectional. Indeed, the immune response can be modulated by various factors such as environmental agents, bacterial products and hormones. Insulin is produced by pancreatic cells and regulates glucose, fat metabolism and cell growth. The action of insulin is mediated through the insulin receptor (IR), localized on the cellular membrane of hepatocytes, myocytes and adipocytes but also on the surface of T cells, macrophages, and dendritic cells. In murine models, the absence of IR in T-cells coincided with reduced cytokine production, proliferation, and migration. In macrophages, defective insulin signaling resulted in enhanced glycolysis affecting the responses to pathogens. In this review, we focalize on the bidirectional cause-effect relationship between impaired insulin signaling and arthritis analyzing how insulin signaling may be involved in the aberrant immune response implicated in arthritis and how inflammatory mediators affect insulin signaling. Finally, the effect of glucose-lowering agents on arthritis was summarized. Frontiers Media S.A. 2021-04-30 /pmc/articles/PMC8119635/ /pubmed/33995414 http://dx.doi.org/10.3389/fimmu.2021.672519 Text en Copyright © 2021 Tripolino, Ciaffi, Pucino, Ruscitti, van Leeuwen, Borghi, Giacomelli, Meliconi and Ursini 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 Immunology
Tripolino, Cesare
Ciaffi, Jacopo
Pucino, Valentina
Ruscitti, Piero
van Leeuwen, Nina
Borghi, Claudio
Giacomelli, Roberto
Meliconi, Riccardo
Ursini, Francesco
Insulin Signaling in Arthritis
title Insulin Signaling in Arthritis
title_full Insulin Signaling in Arthritis
title_fullStr Insulin Signaling in Arthritis
title_full_unstemmed Insulin Signaling in Arthritis
title_short Insulin Signaling in Arthritis
title_sort insulin signaling in arthritis
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8119635/
https://www.ncbi.nlm.nih.gov/pubmed/33995414
http://dx.doi.org/10.3389/fimmu.2021.672519
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