Department of Physiology, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, 90050-170, Porto Alegre, RS, Brazil.
Comp Biochem Physiol A Mol Integr Physiol. 2011 Apr;158(4):400-5. doi: 10.1016/j.cbpa.2010.11.023. Epub 2010 Dec 3.
The present study assesses the effects of osmotic stress on phosphoenolpyruvate carboxykinase (PEPCK), fructose 1,6-bisphosphatase (FBPase) and glucose 6-phosphatase (G6Pase) activities and (14)C-total lipid synthesis from (14)C-glycine in the anterior and posterior gills, jaw muscle, and hepatopancreas of Neohelice granulata. In posterior gills, 24-h exposure to hyperosmotic stress increased PEPCK, FBPase and G6Pase activities. Increase in (14)C-lipid synthesis was associated to the decrease in PEPCK activity after 72-h exposure to hyperosmotic stress. Hypo-osmotic stress decreased PEPCK and G6Pase activities in posterior gills; however, (14)C-lipids increased after 72-h exposure to stress. In anterior gills, decreases in the G6Pase activity after 72-h of hyperosmotic stress and in (14)C-lipogenesis after 144-h were observed, while PEPCK activity increased after 144 h. Exposure to hypo-osmotic stress increased (14)C-lipid synthesis and PEPCK activity in anterior gills. Muscle G6Pase activity increased after 72-h exposure to hypo-osmotic stress; however, no significant change was observed in the lipogenesis. PEPCK decreased in muscle after 144-h exposure to hyperosmotic, coinciding with increased (14)C-lipid synthesis. In the hepatopancreas, a decrease in the (14)C-lipogenesis occurred after 24-h exposure to hyperosmotic stress, accompanied by increase in (14)C-lipid synthesis. Additionally, PEPCK activity returned to control levels. The hepatopancreatic lipogenesis from amino acids was not involved in the metabolic adjustment during hypo-osmotic stress. However, gluconeogenesis is one of the pathways involved in the adjustment of the intracellular concentration of nitrogenated compounds.
本研究评估了渗透胁迫对 Neohelice granulata 前、后鳃、颚肌和肝胰腺中磷酸烯醇丙酮酸羧激酶 (PEPCK)、果糖 1,6-二磷酸酶 (FBPase) 和葡萄糖 6-磷酸酶 (G6Pase) 活性以及从 (14)C-甘氨酸合成的 (14)C-总脂质的影响。在后鳃中,24 小时暴露于高渗胁迫会增加 PEPCK、FBPase 和 G6Pase 活性。72 小时暴露于高渗胁迫后,PEPCK 活性下降,与 (14)C-脂质合成增加有关。低渗胁迫降低了后鳃中的 PEPCK 和 G6Pase 活性;然而,应激后 72 小时 (14)C-脂质增加。在前鳃中,72 小时高渗应激后 G6Pase 活性下降,144 小时 (14)C-脂质生成下降,而 PEPCK 活性增加。低渗胁迫增加了前鳃中 (14)C-脂质的合成和 PEPCK 活性。肌肉 G6Pase 活性在低渗胁迫后 72 小时增加;然而,脂质生成没有明显变化。高渗胁迫后 144 小时,肌肉中 PEPCK 减少,同时 (14)C-脂质合成增加。在肝胰腺中,24 小时高渗应激后 (14)C-脂质生成减少,同时 (14)C-脂质合成增加。此外,PEPCK 活性恢复到对照水平。低渗胁迫期间氨基酸的肝胰腺脂质生成不参与氮化合物细胞内浓度的代谢调节。然而,糖异生是参与氮化合物细胞内浓度调节的途径之一。