Laboratorio de Fisioloxía Animal, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía and Centro de Investigación Mariña-CIM, Universidade de Vigo, Spain.
Laboratorio de Fisioloxía Animal, Departamento de Bioloxía Funcional e Ciencias da Saúde, Facultade de Bioloxía and Centro de Investigación Mariña-CIM, Universidade de Vigo, Spain.
Physiol Behav. 2019 Oct 1;209:112617. doi: 10.1016/j.physbeh.2019.112617. Epub 2019 Jul 15.
To assess the hypothesis that Na/K-ATPase (NKA) is involved in the central regulation of food intake in fish, we observed in a first experiment with rainbow trout (Oncorhynchus mykiss) that intracerebroventricular (ICV) treatment with ouabain decreased food intake. We hypothesized that this effect relates to modulation of glucosensing mechanisms in brain areas (hypothalamus, hindbrain, and telencephalon) involved in food intake control. Therefore, we evaluated in a second experiment, the effect of ICV administration of ouabain, in the absence or in the presence of glucose, on NKA activity, mRNA abundance of different NKA subunits, parameters related to glucosensing, transcription factors, and appetite-related neuropeptides in brain areas involved in the control of food intake. NKA activity and mRNA abundance of nkaα1a and nkaα1c in brain were inhibited by ouabain treatment and partially by glucose. The anorectic effect of ouabain is opposed to the orexigenic effect reported in mammals. The difference might relate to the activity of glucosensing as well as downstream mechanisms involved in food intake regulation. Ouabain inhibited glucosensing mechanisms, which were activated by glucose in hypothalamus and telencephalon. Transcription factors and neuropeptides displayed responses comparable to those elicited by glucose when ouabain was administered alone, but not when glucose and ouabain were administered simultaneously. Ouabain might therefore affect other processes, besides glucosensing mechanisms, generating changes in membrane potential and/or intracellular pathways finally modulating transcription factors and neuropeptide mRNA abundance leading to modified food intake.
为了评估钠钾-ATP 酶（NKA）是否参与鱼类的中枢食欲调控假说，我们在虹鳟（Oncorhynchus mykiss）的第一个实验中观察到，脑室内（ICV）给予哇巴因会减少食物摄入。我们假设这种效应与参与摄食控制的脑区（下丘脑、后脑和端脑）中葡萄糖感应机制的调节有关。因此，我们在第二个实验中评估了，在缺乏或存在葡萄糖的情况下，ICV 给予哇巴因对 NKA 活性、不同 NKA 亚基的 mRNA 丰度、与葡萄糖感应相关的参数、转录因子和与摄食相关的神经肽在参与摄食控制的脑区中的影响。哇巴因处理抑制了脑内的 NKA 活性和 nkaα1a 和 nkaα1c 的 mRNA 丰度，葡萄糖部分抑制了 NKA 活性和 nkaα1a 和 nkaα1c 的 mRNA 丰度。哇巴因的厌食作用与哺乳动物报道的促食作用相反。这种差异可能与葡萄糖感应以及参与食物摄入调节的下游机制的活性有关。哇巴因抑制了葡萄糖感应机制，而葡萄糖在下丘脑和端脑激活了这些机制。转录因子和神经肽的反应与单独给予葡萄糖时相似，但当同时给予葡萄糖和哇巴因时则不相似。因此，哇巴因可能会影响除葡萄糖感应机制之外的其他过程，导致膜电位和/或细胞内途径发生变化，最终调节转录因子和神经肽 mRNA 丰度，从而改变食物摄入。
