补偿生长对异育银鲫IGF-1、IGFBP-1水平及IGF-1、IGF-1RmRNA表达的影响

该实验分析饥饿和恢复投喂对异育银鲫血液IGF-1和IGFBP-1水平和肝脏IGF-1、白肌IGF-1RmRNA表达量的影响。结果显示:饥饿期(14d)血液中IGF-1和IGFBP-1水平逐渐下降,在饥饿第14天均出现显著性降低(P<0.05);恢复投喂后第1天IGF-1迅速恢复到对照组水平,而IGFBP-1水平仍显著低于对照组(P<0.05),随后逐渐升高,直至于恢复投喂第14天后显著高于对照组水平(P<0.05);饥饿期肝脏IGF-1mRNA表达量呈下降趋势,但与对照组无显著性差异(P>0.05);恢复投喂初期(第1、3天),IGF-1mRNA表达量仍继续下降(P<0.05),对营养条件的变化反应滞后,至第7天,表达水平恢复到对照组水平。白肌IGF-1RmRNA表达水平在饥饿第3天出现显著性下降(P<0.05),继续饥饿其水平出现补偿性升高;恢复投喂后第14天IGF-1RmRNA表达量显著高于对照组水平(P<0.05)。该结果揭示恢复投喂期高水平的IGFBP-1含量和IGF-1RmRNA表达量可能通过提高IGF-1的促生长作用参与异育银鲫的补偿生长调节。

Effects of compensatory growth on the levels of IGF-1, IGFBP-1 and expressions of IGF-1 mRNA, IGF-1R mRNA in Carassius auratus gibelio

We studied the effects of starvation and re-feeding on the levels of plasma IGF-1, IGFBP-1 and expressions of hepatic IGF-1 mRNA and muscle IGF-1R mRNA in Carassius auratus gibelio. During the two week starvation period, both the levels of plasma IGF-1 and IGFBP-1 decreased and were significantly lower on day 14 (P <0.05). On the first day of re-feeding, the level of plasma IGF-1 increased sharply, to the level of control group, and had no significant changes for the remaining days. While the level of plasma IGFBP-1 was still greatly lower than that of control group at the first day of re-feeding, it increased significantly higher than that of control group by day 14 (P <0.05). During the starvation period, expression of IGF-1 mRNA in liver decreased, but it was not statistically different from that of the control group (P>0.05). During the early period of re-feeding, the abundance of IGF-1 mRNA was still significantly lower than that of control group (P <0.05), then increased to the level of control group on day 7. IGF-1R mRNA showed a decreasing trend after starvation, and reached a significantly low value on day 3 (P <0.05). After re-feeding, the abundance of IGF-1R mRNA increased to peak at day 14. These results indicate that the higher level of IGFBP-1 in serum and IGF-1R mRNA in muscle after re-feeding could improve the promoting growth effect of IGF-1 to participate in the regulation of compensatory growth.