Role of insulin, insulin-like growth factors, and muscle regulatory factors in the compensatory growth of the trout (Oncorhynchus mykiss)

To examine the various mechanisms involved in compensatory growth in Oncorhynchus mykiss, an experimental protocol involving 1, 2 or 4 weeks of fasting followed by a single ad libitum re-feeding period of 4 weeks was designed for alevins. Morphological parameters including body weight, specific growth rates (SGR), and coefficient factor decreased significantly during fasting. Re-feeding accelerated growth and restored final body weight in groups previously fasted. Plasma insulin and glucose decreased in fasting, while normal levels were restored in all re-fed groups. The expression profile of insulin-like growth factors (IGFs) in liver and of the main muscle growth regulators in white muscle was examined using real-time quantitative RT-PCR. Fasting decreased the expression of IGF-I mRNA in both tissues, while re-feeding restored expression to control values. In contrast, IGF-II expression was not affected by any treatment in either tissue. Insulin- and IGF-I-binding assays in partial semi-purifications (of soluble proteins) in white skeletal muscle showed that insulin binding was not affected by either fasting or re-feeding, whereas fasting up-regulated IGF-I binding. The expression of IGFRIb mRNA in white skeletal muscle also increased with fasting, while IGFRIa increased with re-feeding, indicating that the two receptor isoforms are differentially regulated. The mRNA expression of myogenic regulator factors and fibroblast growth factors (FGFs) was not affected throughout the experiment, except for myogenin, which first decreased and then showed a rebound effect after 4 weeks of fasting. Myostatin mRNA expression did not change during fasting, although re-feeding caused a significant decrease. In conclusion, re-feeding of previously fasted trout induced compensatory growth. The differential regulation in muscle expression of IGF-I, IGF-I receptors, and myostatin indicates their contribution to this compensatory mechanism.