Expression of insulin-like growth factor I in normally and abnormally developing coho salmon (Oncorhynchus kisutch)

Changes in levels of insulin-like growth factor-I (IGF-I) messenger RNA (mRNA) in tissues of normally and abnormally growing (stunted) juvenile coho salmon in seawater were studied. Profiles of hepatic IGF-I mRNA levels were compared with changes in growth and plasma concentrations of GH and insulin. In normally growing fish, IGF-I mRNA levels, as measured by solution hybridization-RNase protection assay, showed that hepatic IGF-I mRNA levels of yearling salmon were highest in May and June. Increased hepatic IGF-I mRNA levels followed increases in both plasma GH and insulin. Levels of hepatic IGF-I mRNA decreased in July, after a sharp decline in plasma GH in June, and remained low until the following spring. The growth rate for normal fish also decreased during fall and winter. After increases in plasma GH and insulin, which peaked in late February, hepatic IGF-I mRNA levels increased rapidly and reached a second peak in April. Increases in plasma GH and hepatic IGF-I mRNA observed in the second year were smaller and occurred earlier than in the first spring in seawater. Growth retardation (stunting) resulted from the premature transfer of cultured fish to seawater. Compared with normally growing fish, these stunted salmon had significantly higher levels of plasma GH but lower levels of plasma insulin. Hepatic IGF-I mRNA levels in stunted salmon were significantly lower, despite elevated plasma GH levels. These results indicate that hepatic levels of IGF-I mRNA in juvenile coho salmon increase in springtime, after an increase in plasma GH and insulin. These seasonal increases in GH and IGF-I precede the rapid growth period coinciding with the springtime increases in temperature and photoperiod and may therefore be associated with these environmental cues. The elevated plasma GH and reduced hepatic IGF-I mRNA levels observed in growth-retarded salmon suggested that stunted salmon may be GH resistant. Hepatic GH resistance and diminished IGF-I production may be the central endocrine defects leading to growth retardation in stunted salmon.