Freitas Flávio Eduardo Dias Araújo, Batista Marcos Adriano Carlos, Braga Daiane Cristina de Assis, de Oliveira Lisandra Brandino, Antunes Vagner Roberto, Cardoso Leonardo Máximo
Dept. of Biological Sciences - ICEB, Federal University of Ouro Preto, MG, Brazil.
Dept. of Food and Medicine - FCF, Federal University of Alfenas, MG, Brazil.
Appetite. 2022 Aug 1;175:106050. doi: 10.1016/j.appet.2022.106050. Epub 2022 Apr 18.
Sodium is the main cation present in the extracellular fluid. Sodium and water content in the body are responsible for volume and osmotic homeostasis through mechanisms involving sodium and water excretion and intake. When body sodium content decreases below the homeostatic threshold, a condition termed sodium deficiency, highly motivated sodium seeking, and intake occurs. This is termed sodium appetite. Classically, sodium and water intakes are controlled by a number of neuroendocrine mechanisms that include signaling molecules from the renin-angiotensin-aldosterone system acting in the central nervous system (CNS). However, recent findings have shown that sodium and water intakes can also be influenced by inflammatory agents and mediators acting in the CNS. For instance, central infusion of IL-1β or TNF-α can directly affect sodium and water consumption in animal models. Some dietary conditions, such as high salt intake, have been shown to change the intestinal microbiome composition, stimulating the immune branch of the gut-brain axis through the production of inflammatory cytokines, such as IL-17, which can stimulate the brain immune system. In this review, we address the latest findings supporting the hypothesis that immune signaling in the brain could produce a reduction in thirst and sodium appetite and, therefore, contribute to sodium intake control.
钠是细胞外液中的主要阳离子。体内的钠和水含量通过涉及钠和水排泄及摄入的机制来维持容量和渗透压稳态。当体内钠含量降至稳态阈值以下时，即出现钠缺乏状态，此时会产生强烈的钠需求并引发钠摄入，这被称为钠食欲。传统上，钠和水的摄入受多种神经内分泌机制控制，这些机制包括肾素 - 血管紧张素 - 醛固酮系统中的信号分子在中枢神经系统（CNS）中发挥作用。然而，最近的研究发现表明，钠和水的摄入也可受中枢神经系统中炎症因子和介质的影响。例如，在动物模型中，向中枢注射白细胞介素 - 1β或肿瘤坏死因子 - α可直接影响钠和水的消耗。一些饮食条件，如高盐摄入，已被证明会改变肠道微生物群组成，通过产生炎症细胞因子（如白细胞介素 - 17）刺激肠 - 脑轴的免疫分支，进而刺激脑免疫系统。在本综述中，我们阐述了最新研究发现以支持以下假说：大脑中的免疫信号传导可降低口渴感和钠食欲，从而有助于控制钠的摄入。
