Next Article in Journal
Beyond Single-Cell Analysis of Metallodrugs by ICP-MS: Targeting Cellular Substructures
Next Article in Special Issue
Opioids and Sepsis: Elucidating the Role of the Microbiome and microRNA-146
Previous Article in Journal
Mammalian and Invertebrate Models as Complementary Tools for Gaining Mechanistic Insight on Muscle Responses to Spaceflight
Previous Article in Special Issue
Effect of Acute and Prolonged Inflammation on the Gene Expression of Proinflammatory Cytokines and Their Receptors in the Anterior Pituitary Gland of Ewes
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

IGF-1 and IGFBP-3 in Inflammatory Cachexia

by
Ana Isabel Martín
1,†,
Teresa Priego
2,†,
Álvaro Moreno-Ruperez
1,
Daniel González-Hedström
3,4,
Miriam Granado
3,5 and
Asunción López-Calderón
1,*
1
Department of Physiology, Faculty of Medicine, Complutense University of Madrid, 28040 Madrid, Spain
2
Department of Physiology, Faculty of Nursing, Physiotherapy and Podiatry, Complutense University of Madrid, 28040 Madrid, Spain
3
Department of Physiology, Faculty of Medicine, Autonomous University of Madrid, 28049 Madrid, Spain
4
Pharmactive Biotech Products S.L. Parque Científico de Madrid, Avenida del Doctor Severo Ochoa, 37 Local 4J, 28108 Alcobendas, Spain
5
CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, 28029 Madrid, Spain
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2021, 22(17), 9469; https://doi.org/10.3390/ijms22179469
Submission received: 10 July 2021 / Revised: 5 August 2021 / Accepted: 28 August 2021 / Published: 31 August 2021
(This article belongs to the Special Issue Molecular Response to Endotoxin)

Abstract

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.
Keywords: GH; IGF-1; IGFBP-3; sepsis; inflammation; muscle wasting; glucocorticoids; cytokines; nitric oxide; cachexia GH; IGF-1; IGFBP-3; sepsis; inflammation; muscle wasting; glucocorticoids; cytokines; nitric oxide; cachexia

Share and Cite

MDPI and ACS Style

Martín, A.I.; Priego, T.; Moreno-Ruperez, Á.; González-Hedström, D.; Granado, M.; López-Calderón, A. IGF-1 and IGFBP-3 in Inflammatory Cachexia. Int. J. Mol. Sci. 2021, 22, 9469. https://doi.org/10.3390/ijms22179469

AMA Style

Martín AI, Priego T, Moreno-Ruperez Á, González-Hedström D, Granado M, López-Calderón A. IGF-1 and IGFBP-3 in Inflammatory Cachexia. International Journal of Molecular Sciences. 2021; 22(17):9469. https://doi.org/10.3390/ijms22179469

Chicago/Turabian Style

Martín, Ana Isabel, Teresa Priego, Álvaro Moreno-Ruperez, Daniel González-Hedström, Miriam Granado, and Asunción López-Calderón. 2021. "IGF-1 and IGFBP-3 in Inflammatory Cachexia" International Journal of Molecular Sciences 22, no. 17: 9469. https://doi.org/10.3390/ijms22179469

APA Style

Martín, A. I., Priego, T., Moreno-Ruperez, Á., González-Hedström, D., Granado, M., & López-Calderón, A. (2021). IGF-1 and IGFBP-3 in Inflammatory Cachexia. International Journal of Molecular Sciences, 22(17), 9469. https://doi.org/10.3390/ijms22179469

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop