Furthermore, the abnormal neuroendocrine response to the prolonged inflammation in RA was characterised by the increased catabolic hormones (i.e. glucocorticoids) and the decreased anabolic factors secretion (i.e. insulin-like growth factor-1) with elevated inflammatory cytokines, leading to hypermetabolism and a marked reduction in arthritic rat body mass [61]. This evidence concerns the gene IGF1 and rheumatoid arthritis.