Rainbow trout with gene editing-induced reductions in serum insulin-like growth factor binding protein (IGFBP)-2b exhibit similar growth performance compared to fish without IGFBP-2b gene disruption. The objective of this study is to determine how the components of the insulin-like growth factor (IGF)/IGFBP system respond to a reduction in serum IGFBP-2b abundance. Editing the IGFBP-2b genes in rainbow trout resulted in an 83% decrease in serum IGFBP-2b in mutants. This resulted in a 35% reduction in serum IGF-I, which was offset by reduced expression of hepatic igfbp-1a2 and increased muscle igfr-1a; these responses suggest that an increased IGF-I signaling capacity offset reductions in serum IGF-I. During feed deprivation, the differential expression of igfbp genes supports the attenuation of the growth inhibitory response, likely due to the further reduction in serum IGF-I that alleviated the need for an IGF-inhibitory response. Unique igfbp expression patterns occurred during refeeding, suggesting an enhanced IGF-I signaling capacity in controls. Collectively, these findings support that the role of IGFBP-2b is to regulate serum IGF-I concentrations. The compensatory regulation of IGF/IGFBP system genes indicates that adjustments in other IGFBP, both circulating and at the local level, maintain IGF-I signaling at a level appropriate for the nutritional state of the fish.
We examined the combined effects of fasting in freshwater and water temperature during the transition from freshwater to seawater on growth/metabolic parameters in juvenile chum salmon Oncorhynchus keta. Juveniles of 1 g in freshwater were first subjected to a 5-day fasting period at 10 or 5 °C, acclimated to either 10 or 5 °C seawater and fed ad libitum for 30 days. Control fish were transferred from 10 °C freshwater to 10 °C seawater and fed ad libitum throughout the experimental period. Serum insulin-like growth factor (IGF)-I was measured to evaluate growth status/potential and liver glycogen as an index of energy storage. Fasting in freshwater for 5 days negatively affected body size. Growth of juveniles kept at colder temperatures was retarded in seawater for at least 20 days, which may partly be explained by a lower feeding rate in cold seawater. Serum IGF-I levels were lower in fasted fish in freshwater at both temperatures and colder seawater had a negative effect on restoring serum IGF-I levels after refeeding for 20 days. Liver glycogen content was low in fish fasted in freshwater for 5 days. After refeeding in seawater for 10 days, liver glycogen content increased significantly in juveniles kept at colder temperatures. Colder water temperatures in both salinities positively affected glycogen content for 30 days after transfer to seawater, suggesting that juveniles allocated energy stores to the liver rather than growth under suboptimal feeding and temperature conditions. The findings of the present study suggested that relatively cold freshwater could negatively affect juvenile chum salmon growth soon after sea entry.
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