IGF-1 and IGFBP-3 in Inflammatory Cachexia

Int J Mol Sci. 2021 Aug 31;22(17):9469. doi: 10.3390/ijms22179469.


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; cachexia; cytokines; glucocorticoids; inflammation; muscle wasting; nitric oxide; sepsis.

Publication types

  • Review

MeSH terms

  • Cachexia / metabolism*
  • Cachexia / physiopathology
  • Growth Hormone / metabolism
  • Human Growth Hormone / metabolism
  • Humans
  • Hypothalamus / metabolism
  • Inflammation / physiopathology
  • Insulin / metabolism
  • Insulin-Like Growth Factor Binding Protein 3 / metabolism*
  • Insulin-Like Growth Factor Binding Protein 3 / physiology
  • Insulin-Like Growth Factor I / metabolism*
  • Insulin-Like Growth Factor I / physiology
  • Muscular Atrophy / metabolism
  • Muscular Atrophy / physiopathology


  • IGF1 protein, human
  • IGFBP3 protein, human
  • Insulin
  • Insulin-Like Growth Factor Binding Protein 3
  • Human Growth Hormone
  • Insulin-Like Growth Factor I
  • Growth Hormone