Receptors for insulin-like growth factor-I (IGF-I) predominate over insulin receptors in skeletal muscle throughout the life cycle of brown trout, Salmo trutta

Insulin and IGF-I binding has been studied in brown trout (Salmo trutta) wheat germ agglutinin semipurified receptors from embryos (organogenesis), larvae (yolk sac), juveniles (2.98 +/- 0.21 g bw) and adults (111.6 +/- 6.92 and 522 +/- 53 gbw). Embryos and larvae were sampled at 5 and 12 weeks after fertilization (December 1999 and February 2000) and juvenile and adults were taken simultaneously (July 1999) and under the same feeding conditions to minimize potential nutritional and seasonal effects. Insulin receptor number was maximal at 12 weeks (144 fmol/mg glycoprotein) and progressively decreased in subsequent samplings. No alterations in affinity were detected (K-d range, 0.21-0.32 nM) and changes in number of receptor paralleled changes in total specific binding. IGF-I receptor number was highest at 5 weeks (1044 fmol/mg) and was significantly higher than values for insulin in all samplings. The affinity of IGF-I receptor did not change (K-d range, 0.11-0.18 nM) but was consistently higher than that for the insulin receptor. A more rapid decrease of IGF-I binding and receptor number was found with age. However, the ratio of insulin/IGF-I binding established in 12-week-old larvae (0.18 +/- 0.01) was thereafter maintained at very similar values in juveniles and adults (0.15-0.17). Tyrosine kinase activity (TKA) for insulin receptors ranged between 136 and 183% and there were no significant changes with age. For the IGF-I receptor, TKA ranged from 174 to 281% and was significantly higher in 5-week-old larvae coincident with the highest levels of receptor number and declined gradually in parallel with binding levels. In conclusion, the greater abundance of IGF-I receptors during embryonic and larval development is maintained throughout juvenile and adult stages. This would suggest a key role for IGF-I in the growth and metabolism of trout muscle. (C) 2001 Academic Press.