2026-06-27T22:42:30Zhttps://docta.ucm.es/rest/oai/requestoai:docta.ucm.es:20.500.14352/50842023-11-22T15:52:56Zcom_20.500.14352_14col_20.500.14352_15
Docta Complutense
author
Martín Velasco, Ana Isabel
author
Priego Cuadra, Teresa
author
Moreno Ruperez, Álvaro
author
González Hedström, Daniel
author
Granado García, Miriam
author
López-Calderón Barreda, Asunción
2023-06-16T14:27:35Z
2023-06-16T14:27:35Z
2021-08-31
1422-0067
10.3390/ijms22179469
https://hdl.handle.net/20.500.14352/5084
https://doi.org/10.3390/ijms22179469
https://www.mdpi.com/1422-0067/22/17/9469
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.
eng
Atribución 3.0 España
IGF-1 and IGFBP-3 in Inflammatory Cachexia
journal article
URL
https://docta.ucm.es/bitstreams/ddd848dd-ade3-4d06-9c74-ac13115edc81/download
File
MD5
73afd04fbcd35436413201f2dd730cfb
979064
application/pdf
ijms-22-09469-v2.pdf