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 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.

Automated summary

Inflammation triggers a broad response from the neuroendocrine system, affecting all the endocrine axes, particularly the hypothalamic-growth hormone-insulin-like growth factor-1 axis. While the endocrine and metabolic responses to acute inflammation support organism survival, chronic inflammation contributes to catabolic processes leading to muscle wasting and weakness. The inhibition of the hypothalamic-GH-IGF-1 axis plays a role in this mechanism.