Departamento de Zoología, Facultad de Ciencias, Universidad de Granada, Campus Universitario Fuentenueva s/n, 18071, Granada, Spain.
CIMAR/CIIMAR-Centro Interdisciplinar de Investigação Marinha e Ambiental, Universidade do Porto, Rua dos Bragas 289, 4050-123, Porto, Portugal.
Fish Physiol Biochem. 2012 Aug;38(4):1145-1157. doi: 10.1007/s10695-011-9600-2. Epub 2012 Jan 7.
The particular metabolic strategies of the common dentex (Dentex dentex) to face a period of prolonged starvation and subsequent refeeding were assessed. Plasma metabolites, endogenous reserves, and the activity of key enzymes of intermediary metabolism in liver, white muscle, and heart were evaluated. Plasma glucose, total lipid, triglycerides, total-, HDL- and LDL-cholesterol, and protein levels, liver, and white muscle glycogen, and perivisceral, and muscle fat were significantly reduced by starvation, whereas liver lipid content was surprisingly increased. Those enzymes involved in phosphorylation and oxidation of glucose and lipid synthesis, as well as alanine aminotransferase activity, were significantly depressed in liver of starved fish. The increase in β-hydroxyacyl-CoA dehydrogenase (HOAD) indicated an enhanced fatty acid oxidation during starvation. Part of the acetyl-CoA generated by β-oxidation was oxidized in the hepatic Krebs cycle, as reflected the increased citrate synthase (CS) activity. The oxaloacetate required for the reaction catalized by CS activity would be supplied by aspartate aminotransferase (ASAT) activity whose activity was also enhanced. Glutamate dehydrogenase also increased to deaminate the glutamate produced by transaminases, especially by the increased ASAT activity. Liver gluconeogenesis of starved fish was maintained at the same rate that in controls, with glycerol playing an important role as glucogenic substrate. The increased hepatic β-hydroxybutyrate dehydrogenase (β-OHBDH) activity indicates that part of the acetyl-CoA arriving from β-oxidation was being diverted for ketone bodies production with dentex liver playing an important role in providing ketone bodies as fuels for other tissues under such circumstances. Most enzyme activities in white muscle of starved dentex were significantly depressed. In heart, starvation induced an important inhibition of those enzymes involved in glucose and protein metabolism, whereas CS, HOAD, and β-OHBDH activities were maintained at control levels. Although several biomarkers assayed returned to control values after refeeding, many others did not, which indicate that after 3 weeks of refeeding, pre-starved dentex is still experiencing a transient period of metabolic adjustments directed toward the restoration of body mass.
研究了普通牙鲆（Dentex dentex）在长时间饥饿和随后再投喂期间特定的代谢策略。评估了血浆代谢物、内源性储备以及肝脏、白肌和心脏中中间代谢关键酶的活性。饥饿导致血浆葡萄糖、总脂质、甘油三酯、总胆固醇、高密度脂蛋白胆固醇和低密度脂蛋白胆固醇以及蛋白质水平、肝和白肌糖原、内脏脂肪和肌肉脂肪显著降低，而肝脂质含量出人意料地增加。参与葡萄糖和脂质合成磷酸化和氧化的那些酶以及丙氨酸氨基转移酶（ALT）活性在饥饿鱼的肝脏中显著降低。β-羟酰基辅酶 A 脱氢酶（HOAD）的增加表明在饥饿期间脂肪酸氧化增强。部分由β-氧化产生的乙酰辅酶 A 在肝三羧酸循环中被氧化，反映出柠檬酸合酶（CS）活性增加。CS 活性催化的反应所需的草酰乙酸可由天冬氨酸氨基转移酶（AST）活性提供，其活性也增强。谷氨酸脱氢酶也增加以脱氨由转氨基酶产生的谷氨酸，特别是由增加的 AST 活性产生的谷氨酸。饥饿鱼的肝糖异生以与对照组相同的速率维持，甘油作为糖异生底物发挥重要作用。肝β-羟丁酸脱氢酶（β-OHBDH）活性的增加表明，来自β-氧化的部分乙酰辅酶 A 被转移用于酮体生成，牙鲆肝脏在这种情况下为其他组织提供酮体作为燃料发挥重要作用。饥饿牙鲆白肌中的大多数酶活性显著降低。在心脏中，饥饿诱导与葡萄糖和蛋白质代谢相关的那些酶的重要抑制，而 CS、HOAD 和 β-OHBDH 活性维持在对照水平。尽管许多测定的生物标志物在再投喂后恢复到对照值，但许多其他生物标志物没有，这表明在再投喂 3 周后，预饥饿的牙鲆仍在经历短暂的代谢调整期，以恢复体重。
