EXPRESSION OF INSULIN-LIKE GROWTH-FACTOR-I IN NORMALLY AND ABNORMALLYDEVELOPING COHO SALMON (ONCORHYNCHUS-KISUTCH)

Changes in levels of insulin-like growth factor-I (IGF-I) messenger RN A (mRNA) in tissues of normally and abnormally growing (stunted) juven ile coho salmon in seawater were studied. Profiles of hepatic IGF-I mR NA levels were compared with changes in growth and plasma concentratio ns 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 p lasma 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 duri ng fall and winter. After increases in plasma GH and insulin, which pe aked in late February, hepatic IGF-I mRNA levels increased rapidly and reached a second peak in April. Increases in plasma GH and hepatic IG F-I mRNA observed in the second year were smaller and occurred earlier than in the first spring in seawater. Growth retardation (stunting) r esulted from the premature transfer of cultured fish to seawater. Comp ared with normally growing fish, these stunted salmon had significantl y higher levels of plasma GH but lower levels of plasma insulin. Hepat ic IGF-I mRNA levels in stunted salmon were significantly lower, despi te elevated plasma GH levels. These results indicate that hepatic leve ls 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 springti me increases in temperature and photoperiod and may therefore be assoc iated with these environmental cues. The elevated plasma GH and reduce d hepatic IGF-I mRNA levels observed in growth-retarded salmon suggest ed that stunted salmon may be GH resistant. Hepatic GH resistance and diminished IGF-I production may be the central endocrine defects leadi ng to growth retardation in stunted salmon.