Aedo Jorge E, Ruiz-Jarabo Ignacio, Martínez-Rodríguez Gonzalo, Boltaña Sebastián, Molina Alfredo, Valdés Juan A, Mancera Juan M
Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile.
Interdisciplinary Center for Aquaculture Research (INCAR), Universidad de Concepción, Concepción, Chile.
Front Endocrinol (Lausanne). 2019 Nov 12;10:779. doi: 10.3389/fendo.2019.00779. eCollection 2019.
Teleost fish are exposed to diverse stressors in farming and wildlife conditions during their lifespan. Cortisol is the main glucocorticoid hormone involved in the regulation of their metabolic acclimation under physiological stressful conditions. In this context, increased plasma cortisol is associated with energy substrate mobilization from metabolic tissues, such as liver and skeletal muscle, to rapidly obtain energy and cope with stress. The metabolic actions of cortisol have primarily been attributed to its genomic/classic action mechanism involving the interaction with intracellular receptors, and regulation of stress-responsive genes. However, cortisol can also interact with membrane components to activate rapid signaling pathways. In this work, using the teleost fish gilthead sea bream () as a model, we evaluated the effects of membrane-initiated cortisol actions on the early modulation of glucose metabolism. For this purpose, juveniles were intraperitoneally administrated with cortisol and with its membrane impermeable analog, cortisol-BSA. After 1 and 6 h of each treatment, plasma cortisol levels were measured, together with glucose, glycogen and lactate in plasma, liver and skeletal muscle. Transcript levels of corticosteroids receptors (, and ) and key gluconeogenesis ( and )- and glycolysis ( and ) related genes in the liver were also measured. Cortisol and cortisol-BSA administration increased plasma cortisol levels in 1 h after administration. Plasma glucose levels enhanced 6 h after each treatment. Hepatic glycogen content decreased in the liver at 1 h of both cortisol and cortisol-BSA administration, while increased at 6 h due to cortisol but not in response to cortisol-BSA. Expression of , and were preferentially increased by cortisol-BSA in the liver. Taking all these results in consideration, we suggest that non-canonical cortisol mechanisms contribute to the regulation of the early glucose metabolism responses to stress in .
硬骨鱼在其生命周期中，无论是在养殖还是野生环境下，都会面临各种应激源。皮质醇是主要的糖皮质激素，参与调节它们在生理应激条件下的代谢适应。在这种情况下，血浆皮质醇水平升高与代谢组织（如肝脏和骨骼肌）中能量底物的动员有关，以便迅速获取能量并应对压力。皮质醇的代谢作用主要归因于其基因组/经典作用机制，即与细胞内受体相互作用并调节应激反应基因。然而，皮质醇也可以与膜成分相互作用，激活快速信号通路。在这项研究中，我们以硬骨鱼金头鲷（）为模型，评估了膜启动的皮质醇作用对葡萄糖代谢早期调节的影响。为此，对幼鱼腹腔注射皮质醇及其膜不可渗透类似物皮质醇 - 牛血清白蛋白（cortisol - BSA）。每次处理1小时和6小时后，测量血浆皮质醇水平，以及血浆、肝脏和骨骼肌中的葡萄糖、糖原和乳酸水平。还测量了肝脏中糖皮质激素受体（、和）以及关键糖异生（和）和糖酵解（和）相关基因的转录水平。注射皮质醇和皮质醇 - BSA后1小时，血浆皮质醇水平升高。每次处理6小时后，血浆葡萄糖水平升高。注射皮质醇和皮质醇 - BSA后1小时，肝脏中的肝糖原含量下降，而注射皮质醇6小时后肝糖原含量增加，但皮质醇 - BSA处理组无此反应。皮质醇 - BSA优先增加肝脏中、和的表达。综合所有这些结果，我们认为非经典皮质醇机制有助于调节金头鲷对应激的早期葡萄糖代谢反应。
