Johansen Katherine A, Overturf Ken
USDA-ARS, Hagerman Fish Culture Experiment Station, 3059F National Fish Hatchery Rd., Hagerman, ID 83332, USA.
Comp Biochem Physiol B Biochem Mol Biol. 2006 May;144(1):119-27. doi: 10.1016/j.cbpb.2006.02.001. Epub 2006 Feb 28.
Rainbow trout, as well as many other species of fish, demonstrate the ability to survive starvation for long periods of time. During starvation, growth rate is decreased and muscle exhibits signs of wasting. However, upon resumption of feeding, accelerated growth is often observed. Alterations in muscle metabolism occur during feed restriction and refeeding, although the ways in which these alterations affect the molecular pathways that control muscle growth have not been fully determined. To analyze changes in muscle metabolism and growth during starvation and refeeding, real-time PCR was used to test the expression of six metabolic-related genes and eight muscle-specific genes in rainbow trout white muscle prior to and after 30 days of starvation, and after 4 and 14 days of refeeding. The six metabolic-related genes chosen are indicative of specific metabolic pathways: glycolysis, glycogenesis, gluconeogenesis, the pentose phosphate pathway, and fatty acid formation. The eight muscle specific genes chosen are key components in muscle growth and structural integrity, i.e., MRFs, MEFs, myostatins, and myosin. Alterations in expression of the tested metabolic-related genes and muscle-specific genes suggest that during both starvation and refeeding, changes in specific metabolic pathways initiate shifts in muscle that result mainly in the modification of myotube hypertrophy. The expression levels of many of the metabolic-related genes were altered during the refeeding period compared to those observed before the starvation period began. However, the accelerated growth often observed during refeeding is likely driven by changes in normal muscle metabolism, and the altered expression observed here may be a demonstration of those changes.
虹鳟鱼以及许多其他鱼类都表现出能够长时间忍受饥饿的能力。在饥饿期间，生长速度下降，肌肉出现消瘦迹象。然而，恢复喂食后，通常会观察到生长加速。在限食和重新喂食期间，肌肉代谢会发生变化，尽管这些变化如何影响控制肌肉生长的分子途径尚未完全确定。为了分析饥饿和重新喂食期间肌肉代谢和生长的变化，使用实时聚合酶链反应（PCR）检测了虹鳟鱼白肌在饥饿30天之前和之后、以及重新喂食4天和14天后六个代谢相关基因和八个肌肉特异性基因的表达。所选的六个代谢相关基因代表特定的代谢途径：糖酵解、糖原生成、糖异生、磷酸戊糖途径和脂肪酸形成。所选的八个肌肉特异性基因是肌肉生长和结构完整性的关键组成部分，即肌调节因子（MRFs）、肌增强因子（MEFs）、肌肉生长抑制素和肌球蛋白。所检测的代谢相关基因和肌肉特异性基因表达的变化表明，在饥饿和重新喂食期间，特定代谢途径的变化引发了肌肉的转变，主要导致肌管肥大的改变。与饥饿期开始前观察到的相比，许多代谢相关基因的表达水平在重新喂食期间发生了变化。然而，重新喂食期间经常观察到的生长加速可能是由正常肌肉代谢的变化驱动的，这里观察到的表达改变可能是这些变化的一种体现。
