Cortisol reduces insulin-like growth factor-1 (Igf1) and alters liver Igf binding protein (Igfbp) and muscle myogenic gene expression in blue rockfish (Sebastes mystinus)

Fish experiencing stressful conditions often show elevated circulating concentrations of the glucocorticoid hormone cortisol, which regulates physiological processes including intermediary metabolism and somatic growth. Prior studies point to cortisol inhibiting growth via changes to growth hormone (Gh)/insulin-like growth factor-1 (Igf1) signaling. However, the mechanisms by which cortisol alters Gh/Igf1 pathways in fishes are not well understood. Here, we explored how cortisol influences growth-related pathways in adult blue rockfish (Sebastes mystinus) by administering a single intraperitoneal dose of exogenous cortisol and examining effects on plasma Igf1 and liver mRNA levels for igf1 and Igf binding proteins (Igfbps), as well as expression patterns of select myogenesis or muscle atrophy-regulating genes in skeletal muscle. Cortisol-treated rockfish had elevated plasma cortisol and glucose concentrations 5 h and 24 h after cortisol administration. Rockfish also showed lower plasma Igf1 concentrations 24 h after cortisol administration, even though relative expression of igf1 mRNAs in the liver was unaffected. Rockfish given cortisol had higher liver mRNA levels for the Igfbp genes igfbp1a and igfbp1b, which encode type 1 Igfbps with proposed inhibitory influences on Igf1 stimulation of somatic growth. Cortisol-treated fish also expressed elevated liver mRNA levels of igfbp2a, −5b and −6, but lower liver igfbp3a gene transcript abundance, as well as reduced mRNAs in skeletal muscle for myoblast determination protein 2 (myod2), a transcriptional activator of myocyte differentiation. These findings show that sustained (24 h) elevated cortisol can lower circulating Igf1 and alter Igfbp expression, which may bring about reduced growth for fish experiencing prolonged stressors.