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.
Highlights
The physiological response to inflammation includes changes in the neuroendocrine system, which helps to combat the aggressor and favors the adaptation of the body to the new situation
Inflammation-induced decrease in the serum of insulin-like growth factor-1 (IGF-1) and IGF-1 binding protein-3 (IGFBP-3) is secondary to an inhibition of their synthesis in the liver, since the liver is the main source of both proteins in plasma
Local IGF-binding proteins (IGFBPs)-3 has been shown to be an inhibitor of cell growth, and it induces
Summary
The physiological response to inflammation includes changes in the neuroendocrine system, which helps to combat the aggressor and favors the adaptation of the body to the new situation. A low-dose intraperitoneal endotoxin injection increases pituitary GH mRNA and serum concentrations of GH, whereas it decreases circulating IGF-1 [3]. Acute LPS administration increases GH secretion, it decreases circulating IGF-1 [6]. Discrepancies between data in humans and rodents can be due to the LPS dose, since authors injected 4 ng/kg to humans [6], whereas in rodents, the LPS dosages employed are between 5 μg/kg and 10 mg/kg (Table 1) Another possibility is that in the acute inflammatory process, the GH response is different depending on the species. In the chronic phase GH, IGF-1, and IGFBP-3 are decreased [11] All these data indicate that in chronic inflammatory diseases, both humans and rodents show an inhibition of GH secretion
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