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IGF-1 and IGFBP-3 in Inflammatory Cachexia
Inflammation induces a wide response of the neuroendocrine system, which leads to modifications in all the endocrine axes. The hypothalamic–growth hormone (GH)–insulin-like growth factor-1 (IGF-1) axis is deeply affected by inflammation, its response being characterized by GH resistance and a decrea...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8430490/ https://www.ncbi.nlm.nih.gov/pubmed/34502376 http://dx.doi.org/10.3390/ijms22179469 |
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author | Martín, Ana Isabel Priego, Teresa Moreno-Ruperez, Álvaro González-Hedström, Daniel Granado, Miriam López-Calderón, Asunción |
author_facet | Martín, Ana Isabel Priego, Teresa Moreno-Ruperez, Álvaro González-Hedström, Daniel Granado, Miriam López-Calderón, Asunción |
author_sort | Martín, Ana Isabel |
collection | PubMed |
description | Inflammation induces a wide response of the neuroendocrine system, which leads to modifications in all the endocrine axes. The hypothalamic–growth hormone (GH)–insulin-like growth factor-1 (IGF-1) axis is deeply affected by inflammation, its response being characterized by GH resistance and a decrease in circulating levels of IGF-1. The endocrine and metabolic responses to inflammation allow the organism to survive. However, in chronic inflammatory conditions, the inhibition of the hypothalamic–GH–IGF-1 axis contributes to the catabolic process, with skeletal muscle atrophy and cachexia. Here, we review the changes in pituitary GH secretion, IGF-1, and IGF-1 binding protein-3 (IGFBP-3), as well as the mechanism that mediated those responses. The contribution of GH and IGF-1 to muscle wasting during inflammation has also been analyzed. |
format | Online Article Text |
id | pubmed-8430490 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-84304902021-09-11 IGF-1 and IGFBP-3 in Inflammatory Cachexia Martín, Ana Isabel Priego, Teresa Moreno-Ruperez, Álvaro González-Hedström, Daniel Granado, Miriam López-Calderón, Asunción Int J Mol Sci Review Inflammation induces a wide response of the neuroendocrine system, which leads to modifications in all the endocrine axes. The hypothalamic–growth hormone (GH)–insulin-like growth factor-1 (IGF-1) axis is deeply affected by inflammation, its response being characterized by GH resistance and a decrease in circulating levels of IGF-1. The endocrine and metabolic responses to inflammation allow the organism to survive. However, in chronic inflammatory conditions, the inhibition of the hypothalamic–GH–IGF-1 axis contributes to the catabolic process, with skeletal muscle atrophy and cachexia. Here, we review the changes in pituitary GH secretion, IGF-1, and IGF-1 binding protein-3 (IGFBP-3), as well as the mechanism that mediated those responses. The contribution of GH and IGF-1 to muscle wasting during inflammation has also been analyzed. MDPI 2021-08-31 /pmc/articles/PMC8430490/ /pubmed/34502376 http://dx.doi.org/10.3390/ijms22179469 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Martín, Ana Isabel Priego, Teresa Moreno-Ruperez, Álvaro González-Hedström, Daniel Granado, Miriam López-Calderón, Asunción IGF-1 and IGFBP-3 in Inflammatory Cachexia |
title | IGF-1 and IGFBP-3 in Inflammatory Cachexia |
title_full | IGF-1 and IGFBP-3 in Inflammatory Cachexia |
title_fullStr | IGF-1 and IGFBP-3 in Inflammatory Cachexia |
title_full_unstemmed | IGF-1 and IGFBP-3 in Inflammatory Cachexia |
title_short | IGF-1 and IGFBP-3 in Inflammatory Cachexia |
title_sort | igf-1 and igfbp-3 in inflammatory cachexia |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8430490/ https://www.ncbi.nlm.nih.gov/pubmed/34502376 http://dx.doi.org/10.3390/ijms22179469 |
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